Hello everyone. I'm Maxwell Skor, biotech analyst with Morgan Stanley. I'm happy to host Sana Biotechnology and Steve Harr, CEO. Before we get started, I just want to read a brief disclosure. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. With that, I'd like to introduce Steve Harr. For those in the audience who aren't familiar, maybe Steve, you can give us an introduction on Sana and any key takeaways. Sure. First of all, thank you for having us. Thank you, Morgan Stanley. Thank you everybody for joining us, both here in the room and online. I'm sure you recognize as well, we're making forward-looking statements. I'll do my little disclosure, which is take a look at our most recent 10-Q filing for risk factors. Sana is approaching now about six or seven years old. We were founded under the idea that one of the most important transformations that will take place in medicine over the next several decades will be the ability to modify genes and use cells as medicines. Our aim is to build a defining company of that era. I don't think there's anything, despite a really difficult operating environment in the cell and gene therapy space, which we can get into why I think that is there and what we need to, how we grapple with it, there's nothing that's dispelled that idea. We set out with really two important goals or ideas. The first is we want to be able to transplant cells. Since the advent of transplant medicine, the major issue that has held the field back has been allogeneic rejection. The way people have gotten around that has been either autologous cells, which are not that scalable, and they don't work for every cell type, or really, really significant immunosuppression. You put someone else's cells into your body, you will reject them. That's been the history of the industry. Part one was we wanted to overcome allogeneic transplant rejection. I'm going to show you or tell you a little bit about it. I think we've done that. I think we've now proven that multiple times in people, and it's been published in places like New England Journal of Medicine and ell and things like that. The second thing we wanted to be able to do was to repair cells. The goal there is to be able to deliver genetic material, either DNA, RNA, even proteins to cells in a specific, repeatable way. What we have shown is that we can do this, it proves clearly, at least in non-human primates, delivering a genetic material in a very cell-specific way. I think it's pretty clear that at least with preclinical data, we have a best-in-class asset. Others are starting to make a little bit of progress in humans, and we need to show that as well in people. Really substantial progress. If you take a step back, where we are with the cell delivery or cell replacement, the most important and exciting area we're looking at is type 1 diabetes. Type 1 diabetes is a relatively simple disease to understand. It's the patient or person's immune system attacks and kills the pancreatic beta cell. The beta cell is the only cell in your body that makes insulin. Up until 101 years ago, it was a death sentence. There was the invention of or the discovery of exogenous insulin. Exogenous insulin helps, but there are 9 million people today with type 1 diabetes, and that's growing. It's supposed to be about 15 million people within 15 years. A person diagnosed with type 1 diabetes has, on average, with the best care, 10 years of less life expectancy. In most of the world, that's 20, 30 years less life expectancy. During that time, they have risks of amputations, blindness, heart attack, stroke, kidney failure. If the sugars get too low, coma or death. If you talk to anybody with type 1 diabetes, they'll tell you that it takes over their lives, right? It's every moment of every day. You're thinking about my insulin, my sugars, what am I, my exercise, what am I doing? We have a really rare opportunity to move forward with what looks like a transformational curative therapy. Our goal with this is very simple: a single treatment that leads to euglycemia, normal blood sugars, with no more insulin, no more monitoring, no more immunosuppression for life. And I think we can comfortably say now this will happen. What, you know, again, we may not do it. We could make a mistake, or we could have safety issues or time, but it will happen. Why are we so confident? As I said, the disease is super simple to understand. It's a missing pancreatic beta cell. About, let's say, 25 years ago, starting with James Shapiro's group in Canada, people started to transplant pancreatic islets from cadavers. Think about an islet as the pancreatic beta cell plus some support cells around it, right? They could isolate islets and transplant those into people with type 1 diabetes. What you saw was you've now seen people out 15, 20 years off insulin and doing quite well. It's not a really scalable or replicable supply source. You also have the challenge that there aren't that many people for whom lifelong immunosuppression is better than lifelong insulin. Over the last few years, you've seen several different groups show that you can take stem cells and grow them or differentiate them into pancreatic islets. Now you have what looks like a more scalable and definitely more replicable supply source. You still have the challenge of immunosuppression. Just within this year, what we've shown is that we can gene modify with the edits we make and get into what they are and why, these cadaveric islets. The first person is making its own insulin for the first time in over 40 years. That data from that patient was actually just published in the New England Journal of Medicine. The official print version came out last week. There's an editorial with it that goes through the mechanism of the drug. It's a transformational finding, right? It's very rare that N- of- 1 gets into the New England Journal of Medicine. I think that now you have all the component parts together to create this curative therapy. What is our goal? We've made a gene-modified pluripotent stem cell. We will grow that into islets. The most challenging part of that for us has been making that first cell that's your drug product forever, the master cell bank. We've now accomplished that. We can get into that. This drug's called SC451. I'm very optimistic that this is a therapy that can reach our goal for people with type 1 diabetes, which is a single treatment with euglycemia and no immunosuppression and no insulin for life. That's the major part of the company. I'm sure we'll get into the other parts. We have this in vivo delivery capability. We also applied the same hypoimmune technology, which is what we use to hide cells from the immune system to make allogeneic CAR T cells. There are a couple of different drugs in development there. But that's a little bit of an overview of what we're up to. That's great. Thank you very much for that introduction. Congratulations on the New England Journal of Medicine publication. Maybe just to level set in regards to the data you've demonstrated to date, how UP421 has informed or translated to the stem cell-derived SC451. Maybe just walk us through the clinical relevancy of what you've shown so far and maybe some of the safety issues that you've overcome. Let's take a step back. This UP421 that you referred to, what we did, what we wanted to figure out was what we're trying to do is gene modify a stem cell. That one single cell will grow into, over time, quadrillion plus cells, right? It's trillions in trillions. It's a billion cells per patient, right? You figure a hundred, a thousand patients in trillion cells. There are 15 million people with the disease seen, right? It's a lot of cells. The most challenging aspect of that has been every time we divide a cell, you get a mutation or two or three. Usually, it's in non-coding regions, and it doesn't matter. What we're doing here is putting cells in growth media that selects for cells equal quickly. We found some clonality would emerge, typically in DNA repair enzymes. A good example of this is I get people in love about things like a TP53 mutation. You don't want to transplant patients with cells that have a P53 mutation. I think that'd just be a bad idea. We've spent a lot of time, energy, and dollars figuring out how to make these cells and grow them through many, many, many, many divisions without seeing problematic mutations emerge. That has been the most important safety aspect that's taken us a long time and a lot of time and energy to overcome. While we were doing that, to go to your question, we wanted to figure out, hey, does this thing, this hypoimmune technology where it's shown it's worked in some humans in CAR T cells, and it's shown that it works in every preclinical model we've looked at, does it translate into the type 1 diabetes space? In type 1 diabetes, you have two problems that you have to overcome. One, allogeneic rejection. Again, put someone else's cells into you, you will reject them. We have to figure out how do we hide it from your immune system. The second is you actually already have a pre-existing immune response to the cells we're transplanting. Even an autologous cell would not work. The patient would just kill it. They have an autoimmune disease. We wanted to ensure that that worked in people. While we were working hard on the master cell bank, we did this investigator-sponsored study in Sweden where we took cadaveric islets, so islets from a recently deceased person, isolated them, and did our gene edits. To see, hey, could we see here that these cells would survive and function? That's all that we were looking for. It was a safety study, a relatively low dose. What we also wanted to see is can we do this and deliver the cells in a different way than what's been done historically? Historically, most islet transplants, what happens is they are injected into the portal vein of a patient, and then the cells are shot up into the liver. The challenges with that are, first of all, it has to be done under interventional radiology. For a disease with 15 million people, it's not that scalable. The second is that when they go into the liver, they tend to cause clots, and because of that, patients are anticoagulated. About 5% of patients actually end up in the hospital either from a clot or a bleed. And again, those are things we don't want. We're trying to really do something that's scalable. The third is a bunch of, you're not supposed to have cells in your body and your bloodstream, and so your immune system will kill them pretty quickly. You want to get on this. We put the cells in the arm. We did gene-modified islets from a pancreas of a recently deceased person and put them into the muscle in the arm of a person with type 1 diabetes. The person's now out. We've shown data out six months. He's making his own insulin for the first time since 1987, and he's doing really well. It's a really exciting outcome. That's not a scalable solution, and so, we're making sure we're working on our scalable solution, which is the stem cell-derived. I think it answers the question, is type 1 diabetes a cure? Will somebody get this curative therapy? The answer is yes. We need to be the ones that put the pieces together. We should be the ones. It's our technology. We need to actually execute and get it done. There are reasons, you know, because we have to deal with safety issues and things like that, and time and capital. We got to make it happen. We can go through what all those are. It was a super important study, I think, for the field of type 1 diabetes. It's a super important study for the field of transplant. It's the first time you've seen really something like this ever, right? Where you can transplant a cell with no other treatments, and in no way they're suppressing the immune system at all, and you see these cells survive and thrive. It's a super important study for Sana. That's great. Thinking about the next phase of innovation at Sana, SC451, I believe you're guided to filing an IND next year at some point. Just thinking about the learnings you've taken so far, how are you going to evaluate durability? Are you going to be doing any imaging? How are we going to understand the viability of these cells going forward? Simplest way to understand the viability is the physical outcome for the person. There are ways to measure what you're doing. When a pancreatic beta cell makes insulin, it actually makes something called proinsulin. When proinsulin is secreted from the cell, it's cleaved into C-peptide and insulin. First of all, C-peptide is relatively stable and measurable in your blood. The amount of C-peptide is a one-to-one direct measurement of the amount of insulin your body is producing. When you inject the insulin, there's no C-peptide, right? The first way you're going to follow this is what happens to C-peptide. Can you find it? Is it at a physiologically relevant level? Does it go up when you eat? Does it go back down when you're not eating? All of those things. The second thing is we want to see these people off insulin. There's no way you get off insulin. You'll die if you stop taking insulin as a patient pretty quickly, right? You're not getting off insulin. That's super easy to measure, right? The third is we will do little sub-studies where you can look at the images of the patient. It doesn't need to be done in every patient. It's a lot to ask them to keep coming in. We'll do PET/ MRIs. In some of them, we showed that where you can actually label, you can actually find beta cells. We see them. It's in that New England Journal of Medicine article. You see them in, in fact, the left arm of the person with type 1 diabetes. We will do all of those things to be able to measure this. It should be relatively straightforward. The durability is something where you're putting in terminally differentiated cells that should live a long time. It should live a long, long, long, long time. Like we have a beta cell we have. Hopefully, this lasts for decades. You're not going to learn that in phase. You're going to learn it over time. You're not going to learn it. I think it's a clinically very relevant drug with relatively short survival. Let's say, I think you'd ask a patient. They'd say, "If I had to have this happen once a year, that's no problem. That'd be awesome, right? I could get rid of the injections of insulin. I could get rid of monitoring my glucose." I don't think that's a good business. We have to, the scaling of these medicines is not simple. We're in no way, do we have a direct path to being able to treat all the people in the world with type 1 diabetes yet. We also have to do it at a cost that makes sense for society. It makes sense for the patient, and it makes sense for our investors, right? All of that has to happen. If that goes to the patient every 6 to 12 months, I don't see that circle being squared. I think that would be not a viable business, but clinically, it'd be super viable. Okay. In regards to the IND filing for SC451, what are the gating factors right now? If you could just level set expectations on the trial design and any feedback you've gotten from regulators. Yeah. Simple IND. You have to do two major things. You have to do a number of things, but one of them is a non-clinical package, which includes GLP toxicology studies and efficacy studies to justify what you're doing. We have to complete all of that with what you would call representative material, right? We've done it. We've actually transplanted with the exact cell line we're using, the exact same starting cell. With a research product, we've done this in mice and seen them 15 months out. It looks great. No histologic abnormalities. They work really well. We have to do that now with what we would term representative material. Finish doing that with representative material is a better way to do it. That's track one. Track two is GMP manufacturing. You move from making it at a research scale and with research quality reagents into making it with a GMP at a clinical trial scale with GMP quality reagents. Those are the two things. You got to get them both done. The latter will happen. It probably just has some time risk to it, right? To safety studies, you have to make sure that adverse things don't happen. The second part of that's a clinical study. I kind of like to think that if your clinical development is super rational and you're changing as few variables as possible over time, a good way to think about the way to start this is this worked with this Swedish study. Why wouldn't you start and try to replicate that where the only real difference is the product itself, right? That's a very broad patient population, but it's not all type 1 diabetics, right? There are certain exclusion criteria in there. Over time, we will work to expand that into younger people, as in 18 and over, into older people. There was an upper limit of age. If you have had a recent heart attack, we don't want to start with that person. If you've had a recent cancer, because if it comes back, that will complicate our understanding that that happened from our drug or from something else. Relatively healthy people who just look at the New England Journal of Medicine paper, that's probably the way to start. It may be a little bit different, but it should be more or less the same. The third, interactions with regulators. I think they've been really constructive. Those are both at the FDA, and I think our very early experience with other parts of the world. I think there's generally recognition that this is a different therapy than anything that's been out there, and there's generally recognition that it can be very transformative. It's different than the interactions we have, for example, with the allogeneic CAR T cell, which are fine, but this is much more productive. It doesn't mean it's easy, but I think it's transparent around what it is that we think we need to do. Before moving on, could you comment at all on the competitive landscape? I think there are Vertex Pharmaceuticals also in this space. Anything you'd call out there? I think for right now, we're kind of in our own competitive landscape in that we're getting rid of, having a simple, if you define the therapy as what we want to is, we want to be able to get patients to have normal blood sugars with no immunosuppression and no insulin. I'm sure others are going to figure it out. There are a host of other companies that are playing around in this space. I'm confident that many of them are really great science companies, and someone else will figure something out. For right now, I think we have a very unique place, and we need to really work urgently to get this into humans and continue to have that. That's kind of where things are. The other thing that we've done, I think, is different than maybe what some others have done. I think one of the challenges of immunology, there are many aspects of immunology that you have to protect against. We actually do have an Achilles heel, right? We have an Achilles heel of if you have pre-existing neutralizing antibodies. The most common thing for that is blood type. I think that's common, really, if you look across all these places. We worked really hard to go forward with an O - line that allows us to be that's a universal donor. I think a lot of the other cell lines that people are working with are limited by blood type because it's just so hard to find these O - donors or lines. We made some ourselves. We brought some, we licensed some in. I think we have a number of areas of competitive advantage. I presume others are going to work really hard because there have been a lot, there are a lot of really great companies that have been playing around in this space for over 10 years that will, you know, at some point, make some progress. For right now, I'm optimistic that we get the chance to at least, you know, figure out if our stuff works for the first time with people. We've got to really, you know, leverage and execute on that lead time advantage. Other people are doing important things for patients. It's just in slightly different, some of the things would be in smaller patient populations, right, or sicker patient populations. For the ones that we're going after, I think we have a pretty unique perspective. Yeah. Just doubling down a bit on that because you hinted at inclusion exclusion criteria for the potential phase one trial. Could you just give us some thoughts on what the target patient population would be initially, and then how you expand that addressable population? Over time, I want every person with type 1 diabetes to be able to get this drug. I've yet to meet a person who has type 1 diabetes who, if they fit this clinical profile, says, "Nah, I don't want it. No, I want to see 15 years of data. I want to see X." It's a very unsatiated patient population. Early on, we'll start with adults, right? We'll quickly move into adolescents, and it will take longer to get into young children. Early on, we will probably, again, not have people who've had a heart attack and things like that, but over time, you want to get this to them. People who have cardiovascular disease, it's so clear that if you get their sugars under control, they benefit dramatically. We will expand it stepwise through clinical development. We're not looking for, we're looking for all comers. It's not like it's people who have poorly controlled type 1 diabetes. Why would you punish somebody? They'll just make it poorly controlled, and they will. If you say, "Hey, you have to have an elevated hemoglobin A1C," I will guarantee you that people will have that hemoglobin A1C within three to six months. If you said, "Hey, you have to have a certain number of hypoglycemic events," that seems like a bad idea, but we won't go down that path. They would find a way to make that happen. It's a pretty unsatiated group of people, and we'd like to make this available to all of them over time. Steve, I think you noted this at the beginning. Maybe you can talk about why it's been so challenging for companies in the cell and gene therapy space of late and what potentially could be a tipping point or an inflection point in the near term. I don't know the tipping point. I think there are two challenges that we're all facing. One is the capital intensity of this space, right? The capital intensity is something where it's not only expensive to make these therapies, but so much of it relates to manufacturing that you are investing a lot of those dollars at risk before you have clinical proof of concept that says, "Hey, this definitely works." That's part one. Part two is we still haven't exactly figured out as a society how or whether we really want to pay for curative therapies, right? You look at the simplest and best example of a scaled cure, which would probably be Gilead's hepatitis C drug. If you were eating, and that was one where through a very short bolus of time, they were able to treat many, many people with a very, very grievous disease. Society really struggled with it, right? In the grand scheme of things, it wasn't that expensive at the end of the day, right? It's just a lot of people. Right now, so much of cell and gene therapy has been for niche populations. Our goal here is to go after a population that's bigger than hepatitis C, right? It's 15 million people. If we happen to go and take care of all type 1 diabetes, this will be really helpful for a lot of type 2 diabetics too, who have very brittle and poorly controlled diabetes. We have to figure out as a society how and when we're going to pay for this. I think those are the two things that sit back and hold you back. There isn't like some handful of examples where you look and you say, "Man, they've built an unbelievably great business so far." I think that's the other challenge. To me, the tipping points come when people begin to make real money from this. Investors wake up and say, "I don't want to miss that," right? The science is moving pretty quickly. I don't think this is a science problem right now. This is a capital problem. Okay. That's helpful. Thank you. Beyond type 1 diabetes, you have a lot of other things going on in the pipeline. Advantages of fusogens platform. Anything you'd like to call out or key near-term readouts that we can expect? The fusogen platform, what this is, is it's a capability to do cell-specific delivery of genetic material in vivo. We chose to go after a couple of cell types early. We did T cells, where I think of what I've really described to you is probably a best-in-class non-preclinical data study, not human primates and things like that. The second is we went after HSCs and to be able to deliver genetic reagents and things like that. I think we have maybe the only thing that's really kind of working there. The third is we did hepatocytes and tons of things with there, so we stopped doing it, right? Within the in vivo CAR T, we made two really big assumptions. One is that cell specificity on delivery matters. We think it matters for two reasons. One is safety, right? You don't need to go into other cells because it just can create toxicities or immunogenicity and things like that. The second is manufacturability. You don't have that many T cells. It turns out if you go into every cell in your body, to get into enough T cells, you're going to have to make a ton of drug that's going in, for example, your liver as well, right? It's both safety and manufacturability. We've done it. We've done this now. We've shown very clearly in non-human primates, as an example, the ability to make a CAR T cell that only goes, but more or less only goes through T cells. It goes to target cell surface target we pick. It's not, you can't find that liver. You can't find it in genetic tissue. You can't find the lungs and things where other technologies show up. And we get, as an example, deep B cell depletion, clean lymph nodes, a B cell reset to all 90 cells, right, afterward. We can predictably get that now in non-human primates. We've shown you a bit of data on that. We'll show you more. I think I can convince you of the data we have that this is something that is pretty good, really good. You've seen a lot of strategic activity happening in this space of late. Our biggest Achilles heel on that is that all of the strategic activity that's taking place is taking place with assets that have a bit of human data. We have a good bit of non-human primate mouse data, but not human data. We most likely need to get that across the goal line. Our challenge is that we're pretty capital constrained, as we talked earlier. I think the type 1 diabetes is such a rare opportunity with such a high-risk adjusted return. It's not that it's a guaranteed return, but a high-risk adjusted return that it behooves us to make sure that we're allocating our capital efficiently to that. Right now, we don't know how we're going to push forward this fusogen platform to get the human data. It may be that we do a bit more work and wait until our cost of capital is lower. It may be that we end up partnering the asset. I could even see that we kind of spin it out into a mostly Sana-owned but partially investor-owned, where an investor can solely invest in that. If we get the data, and either we buy it back or we sell it, the whole thing to someone else. We'll figure out a way to get the right money to it. It is a really promising platform. What you have is this chance from, again, a single therapy at an outpatient, for example, to deliver and make CAR T cells, no lymphodepletion, no chemotherapy, right? A relatively scalable manufacturing process. I don't know if it's fully scalable. You actually don't know the dose. We have something that we think can have a really meaningful clinical benefit for people. We got to figure that out. So just touching briefly on capital allocation, I know you raised recently extended your runway. Any commentary around capital allocation beyond what you've said previously and just your overall runway? Yeah. I'll start. We need more money. I mean, just to be very clear, we're not across the goal line for what we really need. I presume progress will lower our cost of capital over time, but we'll need to raise more money. Whether that's through partnerships, I think non-traditional things or things that haven't been done before, which I think may be available to us. We're working hard on some of them. And/or equity with shareholders. We'll figure that out. From a capital allocation perspective, as I said, we will focus what we need to to get type 1 diabetes across the goal line. We will do that. I would really like to find the capital to push forward this in vivo delivery because I think it's a space that has a lot of important progress being made. There's a good bit of strategic activity. To the extent we just sit on this asset, it's probably losing value, right? We then have a couple of clinical stage allogeneic CAR T cell programs. I think it's pretty clear that they work, at least to some extent, right? We've probably evaded the immune system. Actually, we just published this two weeks ago in a cell journal showing in the human data set their ability to evade the immune system. We do, they do work. I mean, there's an example when you think you see B cell depletion, right? We need to see, do they, are they, I kind of always say, are they okay, good, or great? We'll start with that with the autoimmune study. To me, okay is, yeah, it works, but it's probably not quite as good as an autologous CAR T cell. Good is it works. We have a much simpler and more scalable process, and for both the clinician, for the patient, and manufacturing, right? Great is it's better. The challenge with that is, as I look at the outside world and what you guys are doing, I think there are only two publicly traded, maybe there are three, standalone CAR T companies that have a positive enterprise value. Our challenge is then saying, okay, can we create a data set that both makes investors re-rate the space and declare us the winner from phase I? The odds are pretty low on that, right? We've been very focused on finding a partner because I think that's the best way forward for this asset. I think we can pull it off. If we don't, we may not even go forward with it because I'm not sure the capital allocation is going to make sense in a time period where we have a couple of other very high, we think, risk-adjusted return investments to make. It is something that we're optimistic about. I think it would be good for people and good for patients. If we can do this, it's scaled. It's a scaled process. It works. It's a lot cheaper to make than an autologous CAR T. We need to kind of figure out where this is going relatively soon. Okay. We have been asking a couple of just broader questions to all of our companies. In regards to China's rise in biotech innovation, how are you thinking about your competitive position here? Will this influence your R&D or BD strategy at all? Yeah. I'll start with type 1 diabetes. We just need to get it right. I think we need to focus on our own knitting and not get too distracted by what happens in the outside world. There are two main, I kind of think just broadly what's happening in China is interesting. One, sometimes it's cheaper, right? That cheaper can relate to people cost and just be a bit more scrappy. I think we can do at least as scrappy. Two is there are elements on the regulatory side where they're able to move much faster, right? That's a lot with non-clinical or GLP tox studies, as well as some of the manufacturing. Then you get into people, right? Again, it's the same thing where it's like something that's cheaper, right? Right now, I think we just need to get our own stuff right. I don't know if anybody, there's some faster or I'd say lower bar process that we'd want to embark on related to these, particularly the stem cell-derived therapies. I think this works outside of safety issues, right? Now we've proven all of the components of efficacy. We need to replicate those components that are super important for efficacy and not run into a safety issue. The best way not to run into a safety issue in a person is to get it right in the preclinical setting first, right? I think you also have to remember we're putting in a gene-modified stem cell-derived therapy into a patient population that, but for our therapy, would live for decades most likely, right? We have a high bar we have to meet to justify doing that. I think we need to make sure we test it early. I don't think there's a faster or easier way to do that when you have such a novel technology. A long way away of saying it's really not something that I think we nor our investors should be myopically focused on. We should be aware of, but not myopically focused on. And just. It's different for other spaces, right? Yeah, that's true. Really, and even in the CAR T, every time you look up, there's like another, you run into the problem of what's the right target? If you have the right target, what's the right modality? If you have the right target and the right modality, what's the right company, right? Because you don't know some of those answers, fast matters, fast and cheap matters, right? You see all kinds of times where there's a target with multiple type modalities where people are moving quickly and that some of the Chinese companies are moving quite quickly. In that space, it's very much a part of what we have to grapple with and think about because you see an ability to more rapidly move different modalities into human testing and see, hey, does this really work or not? Lastly, from the regulatory side, is there anything you'd call out as being meaningful or impactful, thinking specifically FDA, MFN, or tariffs? I know we're early, but. Yeah. I think that we're at a stage where the most important aspect of what we think about is the FDA, right? I think that I'd like to think that given the novel in this therapy and the interactions I did, that this would be a constructive relationship. I will tell you, it's not going to be an easy relationship, only in that I think there are a lot of very difficult assays and safety things we need to work our way through. What makes it productive is it's transparent, right? I think that will continue to be the case. We have to make sure we hold a bar in the bargain on that too. MFN, at the end of the day, I think today it's a long ways away. There are a lot of things that could happen. I like to think that we're developing a therapy that has a global price to it anyway. Tariffs, the supply chain is expensive. Adding cost to the supply chain is something that is complicated for us. I hope that those are not permanent aspects of our cost structure. We'll grapple with that as that happens. This is a drug that likely needs to be manufactured at least somewhat proximal to the ultimate end delivery place, at least of end-stage manufacturing. It will be done. If there's tariffs, it will end up being done in the United States regardless. We have a rent. We'll do that for a while here. I don't really worry about it too much. We think a lot about the FDA, and we'd like to maintain our relationship with them. We'll see how that goes. I think that's time. Thank you very much, Steve. Really appreciate your time. Thank you. Thanks, everybody.