Pushkin. Rick Slayman is sixty two years old, lives in a suburb of Boston, works for the state Department of Transportation, and about five years ago he got a kidney transplant. Then last year his new kidney stopped working, his health declined. His prognosis was pretty bad, so earlier this year, he and his doctors decided that he would be the first person in the history of the world to get a
kidney transplant from a genetically engineered pig. Surgeons did the transplant on March sixteenth, and two weeks later, Rix s Layman walked out of the hospital. It's still too soon to say how he'll do in the coming months, but as of this recording, he's doing well. I'm Jacob Boltstein and this is What's Your Problem, the show where I talk to people who are trying to make technological progress.
My guest today is Mike Curtis. He's the CEO of Egenesis, the company that bred the genetically engineered pig that provided the kidney for Rick Slicker. Every year, thousands of people die waiting for an organ transplant that never comes. And so Mike's problem is this, is it possible to genetically engineer pigs to provide organs, kidneys, livers, hearts for people, and in the long run, is it possible to make pig organs that work even better than human organs for
human transplant patients. So for a really long time, right, like hundreds of years, people have had this idea of transplanting organs or skin from animals to people, like where do you where do you date the beginning of this idea too?
It was it was even pre dated human human transplants. So as soon as you know, physicians realize that organs can fail, I think the first instinct was can we get them from somewhere else? Right? And in the early days of that horribly right, no, no good success. So we kind of pre you know, date that to the dawn of modern medicine. And nothing worked.
And nothing worked because basically the human immune system rejected the transplants.
And that was before we even knew what that was.
But right, yeah, And so to jump forward a very long way, it seems like Crisper, this ability to edit genes is sort of a key breakthrough.
Is that the kind of key moment that enables this new era that seems to be beginning right now?
Absolutely. There were some challenges in the cross species transplant that just unresolvable until the discovery of Crisper. So the one that we took on was in the nineties, it was discovered that poresign retroviruses that are indigenous in the genome, so they're kind of embedded in the pig genome, could infect human cells. And in the nineties, you know, we were coming out of the HIV epidemic, and we did not want to, you know, cause another problem. So we
didn't want to have a cross species zoonotic event. So in many countries around the world they put a moratorium on cross species transplantation because of this risk of indigenous retroviruses.
And so I just want to pause here because I didn't know about indogenous retroviruses until I started preparing for this interview, and it totally blew my mind that there is such a thing. Right, So, an indogenous retrovirus, as I understand.
It is.
Not like a disease that a that an animal has in this case, a poor sign. Indogenous retrovirus obviously is an indogen retrovirus in a pig, and it doesn't mean that the pig is sick It means that in the genome of every pig there is genetic code to code in that pig a retrovirus, right, And similarly, in humans there are other indogenous retroviruses. We have in our genome the code for retroviruses, that's right. Why why do mammals have the code for viruses in our genomes?
Yeah? What's interesting because there are some functions that are ascribed to these indigenous retroviruses. So they kind of co evolved, you know, with pigs with people, and they pick up some function, right, And so we don't completely understand why they're there, but they're there and they pose a risk, right, an infectious disease risk to patients, especially when you think about patients who might be under immino suppression.
And so, just to be clear, just I won't I don't want to be labor this, but it is really
extraordinary coming to it new. The notion is a very very very long time ago, some pig in this case got infected with a virus and that virus made its way into the genome of essentially all the pigs living today, and that genetic code is not harmful to pigs, but there is a fear that if you took a pig kidney, say, and put it in a human being, the code for that virus, which is fine in pigs, might be harmful in people.
Exactly. It's an unknown risk, ye.
And so in the nineties, particularly as you said, in the context of the fear of HIV, people are thinking about doing could we transplant a pig kidney into a human and regulators essentially are saying, well, one reason you cannot do it is because of these endogenous retroviruses in the pigs DNA.
Exactly, and we can't quantify the risk, and so we don't know what will happen, and we actually don't want to know. You need to come up with a way to mitigate the risk of retroviral transmission from the donor to the recipient.
Okay, And so that's just like a red light, do not pass. Go stop doing this for a while. Once that happens.
In the nineties, exactly, most of the people that were investing in the space stopped investing in the space. The progression towards clinic stopped. It really slowed the whole field down because no one knew exactly how to quantify the risk or then what to do about it. And so any pig genome you'll have between fifty and seventy copies
of the retrovirus scattered throughout the genome. And so even if you wanted to go in and remove them, there was no technology available that would allow you to do that. And no one knew of a way to actually actively get rid of these viruses right until the discovery of Crisper.
So Crisper comes along what ten issuars twelve years ago, and it's this incredible technology for editing a genome. Right, people think, oh, maybe we could solve that poresine and dogenous retrovirus problem using Crisper.
Yeah, so this is what George Church kind of took up at Harvard was like, it kind of what would do we use chrispher for? And this this problem was out there and George took it on and said, well, let's see if you can inactivate all copies of the retroviruses in the pig geno. The beautiful part about Crisper is once you give it a sequence, right, it will edit all copies of that sequence in a given genome. Now, the worry was that you would then create basically Swiss
cheese out of the genome. Right, you would create an unviable genome. There's too many edits, was the original thought. But George and the team at Harvard showed that no, you could actually inactivate all copies of the retrovirus and then produce a viable pig.
Right, because I suppose the other question is like, even if you can cleanly make all the edits, do does the pig actually need this indogenous retrovirus for a reason we don't understand.
Right, And we know it does if you if you completely knock it out or get rid of it, the pigs are not healthy. So we make a relatively subtle change to the viral genome that that prevents the virus from replicating. So with this edit, the virus can no longer replicate hot.
But so you don't knock it. You don't entirely remove the sequence from the genome.
You just.
Edit the genome such that this virus, once it's expressed, cannot replicate.
Right, So essentially inactivate those of Dodges viruses.
And so this idea from George Churchill was one of the like giant names in genetics. Right famous scientists was that the origin of the company.
So it came from from from George's lab and we we one of his postdocs started Egenesis by outlcensing the technology from Harvard. So the original idea was to start Egenesis with the idea of making animals that were retroviray inactivated and then also do the rest of the editing right that made the pigs more compatible with human recipient.
So that's how we got into the field. And then from the from then we've built the additional editing to provide organs that are more compatible with first non human primates and then now with people.
So you have inactivated the endogenous retrovirus in the pig. This is like step one, right, But at this point, if you tried to take that kidney, even though you've solved the retrovirus problem, it's still a pig kidney, right, and the human body would know that and would not accept it. So what do you have to do next?
Sure, and so if you just took an unedited pig kidney and try to put it into a monkey or to a person, to be rejected within minutes. And that's primarily due to what we call hyperacute rejection, where the humans are recognizing the carbohydrate differences between pigs and humans. So carbohydrates are that coat all the cells, and humans have antibodies that can recognize those pig sugars. So what we do is we inactivate three genes responsible for those
carbohydrate differences between pigs and humans. Once you do that, we create what we call the triple knockout. So we inactivate those genes, knocking out those carbohydrate differences and eliminating hypercute rejection.
And when you create a pig with those particular carbohydrates eliminated, does it matter to the pig? Is the pig sicker?
As a result, we haven't seen any impact on the health or longevity of a pig. So, for instance, we have several animals in our colony that are a couple of years old, and so we haven't seen any effects on the longevity of those animals. So no, we haven't seen any downside.
Okay, so you've inactivated the endogenous retrovirus and now you've eliminated the carbo hydrates that are causing acute rejection. There's like one more set of changes you've got to make, right, That's right.
So what the field has shown over the past forty years. Is that if you add human genes to the pig genome, you can help regulate different areas of incompatibility. So when we think about, for instance, coagulation, right, So the coagulation factors in the pig are not one percent compatible with humans, so we introduce human coagulation factors into the pig.
Coagulation factors just what causes the blood.
To clot basically or prevent the blood from clotting? Yeah, either way, both both corrections, yep, absolutely. And then we also add regulators of complement activation. The first kind of immune response that you're going to get to a graft in a transplant is what we call compliment activation, and that leads to loss of cells, right, and that leads to death of cells. But by introducing human complement regulators into the poor scine tissue, we can slow down or
quiet that complement response. And then we add module later of what we call the innate and adaptive immune response. In total, we add in the animal that was used in mister Slamon's transplant, we introduced a total of seven regulatory human proteins. So if you add it together, it's fifty nine edits to inactivate the retroviruses three edits to improve the carbohydrate compatibility, and then seven edits to introduce human regulatory trans genes, for a total of sixty nine edits.
So it's basically the first two categories are make it less like a pig, and then the third category is make it more like a person.
Yeah, that's a good way to think about it.
That's right, And I mean presumably at some margin you want to make it as little like a pig and as much like a person as possible. But the pig still has to live, to grow up and have a kidney.
Right, absolutely, And we've produced animals with more trans genes without any issue. But you can imagine at some point, right, you'll reach a point where the pig no longer can tolerate whatever the editing you're doing. We're actually already impressed that we can produce healthy, viable pigs with this number of edits. If you go back ten fifteen years, nobody thought that you could viably do this. Even in activating
fifty nine copies of the retrovirus. Many felt that that was too many and the genome wouldn't be able to handle it. We can tell you that it's not easy, and it's not trivial to do it. It took us a lot of time to figure out how to do it, but now we've shown it it is doable.
I'm sure that it's not easy, but I don't know enough to understand, like what's hard about it? Like tell me a thing that you had to figure out.
Sure, so when you do that much engineering to the genome, you can get aberrations in the genome that prevents you from making a pig. So one of the things that we do is we do what's called clonal selection. So we'll engineer thousands, tens of thousands of cells and then select genomes based on viability. So, for instance, to so produce our seventeen eighty four donor, we had to screen over four thousand clones to find clones that had the adequate quality of genome to then make pigs.
Huh. So let's just let's just talk about that for a minute, like how that actually works, which is the more basic question of just how does the whole thing work? Like I get in a sort of abstracted space what you're doing, but like in whatever in a you know, in a cell, fundamentally there is a cell, right like, what are we starting with.
So we'll take a sample of skin from an adult what we call wild type so unedited pig. Then culture those cells, make many cells, and then those are the cells that we're going to edit. So those are the cells that we take crisper. We make the fifty nine edits, we make the triple knockout, and we make the seven trans geens. In the case of the seventeen eighty four animal, we did that through three sequential routes.
So just to be clear, the seventeen eighty four animal, this is like one particular pig, the pig that donated the kidney that is in a person right now.
So that's the seventeen eighty four refers to the genetics. So we make many seventeen eighty four animals. So it's a particular.
Edited genome, and it's the edited genome that you have described to me.
Yeah, exactly, okay, right, So to make that animal, we actually went through three rounds of editing, right, So we would make the retroviolent activation make a pig, then take those cells, edit them to make the try add the truckle knockout, make a pig. Then we come back and add the seven trans sheats.
So it's multiple generations. You're you are sort of adding changes genetic mutations over successive generations.
Exactly why this allows us to select right. So there's there's two there's there's two restrictions the time. Because we're working with primary cells the time, you have to edit them before they what we call sinat. So at some point those cells stop dividing. You need to edit while the cells are still divide, so you have a limited number of days to do the editing, right, So we do. So this is why we were doing three rounds of editing, because we can get the retroviral in make a pig,
we can get the triple knockout make a pig. We get the seven genes and make a pig. What's really important to that whole process is at the end of each editing round, we then screen individual cells for the genotype. Right, And this is where we'll go through and screen you know, up to four thousand cells to pick cells that look like they have a good morphology and a good phenotype
for which we would then make a pig. So, once we do the editing, we then pick individual cells that we call clones, and then we grow those clones out, and now we have an edited porsone genome, but we still don't have a pig.
So you basically have a whatever, a petri dish full of pig skin cells that have the genotype that you want, exactly, okay.
And so now we need to make a pig. And the technology we use to turn a single cell into a pig, it's called a somatic cell nuclear transfer. It was similar to tchnology that was used to clone Dolly, where we take the nucleus of the edited cell and basically transfer it into the O site of a pig.
An egg cell. And and so this is now a whatever thirty year old technology that they used to clone a sheep with in the nineties exactly.
There's been some obviously improvements since then, but the core idea is essentially the same. And then we use that cloning technology to then make pigs. So we make an embryo and then we transfer that embryo into a surrogate sal and then that surrogate sal will carry the piglet to term.
There's some ethical dimension to this, like like, what are the relevant ethical dimensions to you?
Yeah, our focus is on preserving human health and saving patients who are dying on the transfer wait list, and we believe that this approach is justifiable with that goal in mind. So every day we show up, we focus on patients like mister Slayman. And so this is a means to an end. This is a means to producing organs that currently don't exist. It's to save paces who
are imminately dying, but they are. It's a very bleak outlook for some of these folks, right, And so we view that the work that we're doing for engineering the persa and genome and producing compatible organs all about, you know, realizing that mission of helping these patients, and we believe that that puts us on a very firm ethical route.
Still to come on the show, how pig hearts might help human babies. How many pigs with this genetic sequence are there?
You have about fifty or so animals that are at different ages.
So, like, do you have a farm somewhere?
So we do. We have two farms we have and they are both out in the Midwest. One is a research more of a research farm. It's a two hundred acre farm where we institute biosecurity. So one of the keys here is to produce animals that are free of pathogens that could put harm to either the organs post transplant or the patient or the recipients. So that farm
produces relatively clean animals. But then we have what we call a clinical grade or designated pathogen free facility where the animals are growing inside what we call a barrier. So there we control feed, water, everything that comes in to try to keep pathogens out. So we're actively managing
the environment that those animals are raised in. And on top of all of that, we're doing very robust path consistent pathogen testing, so we're constantly monitoring all the animals for any potential pathogens or disease.
Right, I mean presumably some kind of like jumping the species barrier or transfer would be one of the like nightmarishly bad outcomes, right.
Yes, I mean one of the reasons that we selected pigs as the species is one we've co you know, existed with these animals for thousands of years and we haven't seen that you know, that particular that type of disease transmission, and then we can edit, and then we also know how to grow animals at scale. But yes, we're always on the lookout and I think this is part of surveillance that we'll do for the foreseeable future, is on the lookout for things that we aren't paying attention for. Right.
So let's talk about the first patient. Let's talk about Richard slam and the first person ever to be walking the earth with a pig kidney as far as we know, probably.
Why him?
What was it about his case that made him the right patient?
Yeah, So it's a great question, and part of it was inspired by the work that was done at the University of Maryland in the first heart transplants, right, so we refer to those as the Bennett and Fossett transplants.
The first pig heart pig heart, Yeah, which just happened. That was like a different project, right, but it just happened in the last year or so, right now, the.
Last two years two years, Yeah, absolutely. And there was always this debate in the field of zeno is what patients would constitute the right patient population to go into And the team at Maryland really showed us that there's a case for compassionate use. There's a case for patients who have reached the end of the treatment options and really they're facing imminent death and we have a technology
that could save their life, so shouldn't we try now. Unfortunately, you know, those gentlemen passed away within forty or fifty
days post transplant. But it showed us that the regulatory agencies were open to the discussion, and we just need to define what is the right patient population in the case of kidney and so we had a discussion with the FDA back in twenty twenty two about what would be the right patient population for a formal phase one clinical study, and we'd come to agreement on patients over fifty, patients on the transplant weightlist, and patients that had failed
a previous alo transplant, right, so they'd had a human kidney before, and they had it for a certain duration of time and eventually that kidney fails and you find yourself back on the transplant weightlist. And why that patient population made sense is because those patients have a very low likelihood if you're over fifty with that profile of getting a second kidney. Now, in the case of mister Slamon, are patients like him. He was also losing access to dialysis,
so he had a kidney transplant in twenty eighteen. He had been on dialysis for seven years, got a kidney transplant, the kidney function for five years, and then he lost the kidney stop functioning. In twenty twenty three, Okay, he found himself back on dialysis, but he was having trouble with vascular access, so he had to go through multiple surgeries to create access so he could go on dialysis.
And just to be clear, dialysis is when your kidneys don't work. There is a machine and they hook you up to the machine and it cleans your blood. It does the work of the kids.
Yeah. Usually, you know, the typical schedule would be three times a week, four hours each time.
Okay, And so Richard Slaman, you were saying dialysis just wasn't working for him anymore.
In some patchion it was just very hard to do. It was working, but he would have to have these vascular access surgery so his blood vessels would acclude and prevent the ability to do dialysis. So we'd have to go through a relatively painful procedure to allow him to get dialysis. And I think, you know, he was and I think his neuprologist, when Williams put it really well, he was kind of losing faith, losing hope, like, huh,
is this my life? Is this my future? Like, I'm just going to have to keep doing this and I have no chance of getting a transplant because he had had a transplant for five years, so he knew what that was and now he finds himself on dallasis. So, so we knew at some point mister Sliman would lose access to dialysis and without a transplant, he would he would go to hospice. And so he was a patient
that we felt was a good candidate for trying. And so the team at Mass General approached mister Slaman with this idea of he could participate and be the first patient to try this, and this is what we knew, and these were the risks, and I think that's part of one of the biggest challenges, kind of articulating what we know and then articulately what we don't know and how this could go. But much to mister slam his credit, right, he was the one that raised his hand and said
he would go first. And then we took it to the FDA and we laid out the case to the FDA that you know mister Slamon's story and kind of where he found himself in his treatment. What we had been doing are non human primate data, all the data on the characterization of our donors. And after a few weeks of discussion, the FDA said, we agree and you guys can try.
So what is the path for you for your fore genesis?
From here, we believe that there's the opportunity to treat more patients like mister Slimon. He's not unfortunately, he's not unique in this space, and there are other patients that are suffering very similar fate with continued success. Our intention is to do more of these expanded access requests and transplants while we prepare for a formal trial, right so in patients that may be facing less risk than patients like mister Slamon, patients earlier in their dialysis journey, earlier
in their their kidney failure progression. But that will come, you know. Our intention is to file something like that at the end of twenty twenty five. Beyond that, you know, we are also exploring patients that are suffering from liver failure as well as heart failure. This past December, we did the longest liver perfusions on liver perfusion in a decedent patient. Ever, we did three days of continuous perfusion.
The idea there is you take a patient who may be suffering from liver failure and perfuse them through a pig liver to allow their own liver to recover again. This was something that was demonstrated in the nineties to work. So they took fourteen patients with acute liver failure perfused them through pig livers. All fourteen patients improved. Seven patients were successfully bridged to transplant.
So just to unpack that for a sec the pig liver is kind of like when people get put on those like external artificial hearts or something like the outside the body, and it's like or.
What you know when think about kidney disease is akin to dialsis right? You hooked up to a machine. In this case, in the machine is a big.
Liver, and like, is it in a box?
Like yeah, yeah, So it's in a plastic container on a perfusion device.
So the pig's liver is doing the work of the liver for the patient while the patient is waiting for a human donor exactly. Like, let me ask the dumb question, why not just put the pigs liver in the person.
Because the incompatibilities between a pig liver and the person are still too great. OK, So we could I think we're only going to get a week or two before that gets rejected.
And so similarly, does the perfusion just last for a week or two it's just like an emergency bridge.
Yeah, so it's a great question, and we started out with a goal of greater than twenty four hours of perfusion. The pen study went for three days. Looking at the histology at the end of the study, we believe it can go for about a week. So we're continuing to push the duration.
So that's like a that feels like much more of a kind of edge case than the kidney case.
Well, this is the thing. We think there's actually much greater unmet need and liver failure than there even is in kidney failure because these patients, because there is no equivalent of dialysis, they either recover on their own, which is a little bit of like ICU time and hope, or they get transplanted. So we're hoping that we can provide liver support through a poresigne liver, we can bridge more patients to recovery.
Okay, and then you're and then hearts.
Yeah. So the third setting, again is inspired by the work done at Maryland, but instead of looking at adult patients where the heart has to and heart has to function continuously or the patient passes away, we're focused in the pediatric population. So children who need a heart transplant currently have poor standard of care to bridge them to human heart transplant.
And so this is like typically like babies born with genetic anomalies.
Yeah, typically children under two is kind of where the focus is and the current support of care. About fifty percent of these children die waiting for a human heart transplant.
That is a brutal one. Is a brutal That would be a good one too, Yeah, that would be a good one to tve.
And so the idea is if we can simply create one hundred to two hundred day bridge using a Poresigne heart, then at the end of that or sometime in the middle, when the human heart became available, the child would simply get the human heart. So we call that a bridging strategy.
And so in that instance, is it a transplant or is it external It's a transplant.
Yeah, So the intention is to do the por signed heart transplant allow the patient to go home. They can wait at home right now, they would have to wait in the hospital, but they could wait at home until the human heart becomes available.
Okay, So so those are two other organs. When do you think you're going to do those?
So the intention, the intention is to do all that this year, right, So, we believe we have the not what we call non clinical data or the primate data to support moving into the clinic. And I do think mister the success so far with mister Slaman's transplant is helpful because the emune of suppression that we plan to use in the pediatric heart setting is very similar to
what we're using in mister Slaman's transplant. So we do think that continued success in the kidney transplant will help inform what we're going to be doing at heart.
And is it the same set of genetic changes?
Yeah, so it's the same genetics of the donor. So the current plan is to use the same donor for both kidney, hearts and livers.
And how does how does the immune response to a pig organ compare to the immune response to an organ from another human?
Yeah, it's definitely more robust.
More robust meaning worse in this concept, it's.
Probably going to require you know, we already are using more evenie suppression. Yeah.
And is there some medium to long term future where you do more gene editing in order to make that piece of it easier, where you make the pig kidney more like a human kidney.
Yeah. Absolutely. The long term vision here is to produce organs that don't require immuno suppression, party.
That don't require it at.
All at all. I mean, that's the ultimate that's the vision.
I mean, if you could do that. Just to be clear, like that vision is a pig kidney is better than a kidney from another human.
Right, I mean it sounds like you've been talking to George. Wow.
I appreciate that you were skeptical. You were supposed to be high picking up and I'm supposed to be skeptical. No. But if you say, like, is that even plausible? I appreciate that you're skeptical of it. That's good.
Yeah, do it might work for me. I think one of the things that transplant World has taught us over the past fifty years is things that we thought were impossible are actually now routine, right, So I think it's a matter of time, effort, and work. I think we
can get there, right. I think this initial transplant into patients is a really important step because for us to be informed about what we need to do from an engineering perspective, it is very helpful to have data from humans to feedback into that loop, so we can do
lots of things from an engineering perspective. The question is what to do next, and I think the results that will achieve with mister Slayman and patients like him will help inform what else we need to do to really realize this big vision, which is organs that don't require suppression.
Organs that don't require suppression, is wildly ambitious, right do you? I mean it seems like, not knowing basically anything about it, it would be a kind of incremental, maybe even as symptotic, like, ah, this will get us to less, This will get us to less as opposed to some binary breakthrough. Does that seem right?
Yeah? I think it's incremental. But what we're starting to see is kind of multiplex editing in a way that we couldn't even before Christper, we couldn't conceive of making fifty nine edits for GENO. Okay, now we're conceiving of how would you make a thousand edits to geno? What does that actually look like? And I think that's what's going to be required. Huh.
I mean, do you get weird like structural like three D structural problems once you start doing that, like is it even gonna yes work?
So there's definitely a lot to solve, right, So how do you make you know, how do you make that many changes without totally destroying the geno? We thought that originally with Crisper and the first retroviolent activation, they thought you would never be able to make that many at it. So we did that. We just have to figure out how to do it. And you know, we don't know how to do it right now, but I do think we'll figure out how to do it.
We'll be back in a minute with the lightning. Let's finish with a lightning ground. I won't take much more of your time.
Okay, Okay, what's one.
Thing that that we don't understand about the human body that you wish we understood?
I think, coming from the neuroscience world, I think we have a really poor understanding of mental health and what to do about depression, and because I think those are just paralyzing diseases that we are a long way from really understanding why they exist and actually how to effectively treat them. So if you could generalize that as brain, we still don't really understand in the way we need to, you know, how the brain actually works and what we can do to improve diseases of the brain.
Well, I know you worked in pharmaceuticals for decades, right, I don't point on it, Yeah, and so you know it's a famously hard industry. Most drugs fail, right, I'm curious if you have any any tips for dealing with failure.
I think you go in with the best hypothesis, you run the most efficient studies you can, and then you pick yourself up and go again, because I think you can't let failure bring you down, right, And we know we're going to fail, and often we learned a tremendous amount from those failures and we just have to build on them. The worst thing you can do is stop. I think you have to always keep going.
So if you look back over the thirty years that you worked in the drug industry, I'm curious, like, if you think about when you were getting into the field. What is something that has happened since then, like a breakthrough, a change that you wouldn't have expected that's surprising to you.
I think this whole field of genetic medicines, you know the fact that we're now producing potential cures for sickle cell, cures for beta thalsemia. I think those were all visions that we had, you know, fifty sixty one hundred years ago, like could we actually cure diseases that we're now literally on the shelf have cures for. And I think that no one ever thought we would get there, and here we are.
So conversely, so that's the happy surprise. Is there something when you got into the field that you fought like, surely we'll figure this out, Surely this will be solved that we haven't figured out.
I mean, our inability to really effectively fight viral infection is, you know, our infectious disease broadly. We really haven't evolved our armamentarium against infectious disease very much. I think there we've way under invested and focused on infectious disease. I don't think the current way we fund drug development doesn't support active work there. I think it's the one. It's a blind spot for us, and I think we saw it, you know, during COVID.
Yeah, right, so.
And it's still a blind spot. What's really sad is I don't think COVID. Actually, I don't think we've done much different than we were.
Doing that that that hurts, but I think it's true.
Mike Curtis is the CEO of E Genesis. Today's show was produced by Gabriel Hunter Chang. It was edited by Lydia jene Kott and engineered by Sarah. You can email us at problem at Pushkin dot FM. I'm Jacob Goldstein and we'll be back next week with another episode of What's Your Problem.