Welcome, everyone, to the 44th Annual J.P. Morgan Healthcare Conference. My name is Tess Romero, and I'm one of the Senior Biotech Analysts here at J.P. Morgan. Our next presenting company is Wave Life Sciences, and presenting on behalf of the company, we have President and CEO Paul Bolno. Paul, over to you. Thank you, Tess, and thank you, everybody, for joining us today. Before we start, we'll obviously be making some forward-looking statements during this call, so I'd please ask you to refer to our SEC filings for updates. Taking a pause and thinking about entering 2026, we are energized now more than ever to unlock the broad potential of RNA medicines and open up the opportunity to transform human health. And what this really reflects back on is a journey on building a leading RNA medicines company. And at the foundation, and this is going to be important as we speak to the evolution of the clinical portfolio, is the foundational bedrock of Wave is in our RNA chemistry. So when we talk about what we've been able to build and differentiate from, we should be thinking about a proprietary chemistry engine, and we'll share more on that later, that enables us to rapidly take deep genetic insights and translate those into impactful medicines. And I say this because the speed with which now we can take chemistry and translate that into medicines is incredibly rapid. So to put this in context for the obesity therapy, it was 18 months from the time we generated mouse data to human clinical data and about 24 months from the time we had identified a genetic sequence to deliver clinical data. So rapid insights into rapid medicines. This is all built off of a foundational broad IP estate and, importantly, translates to the building that we've done in manufacturing. So therefore. Oh, with the. And so with our own in-house GMP manufacturing, we've been able to rapidly translate medicines forward, and we'll talk about how that's been important as we advance in the clinic. Taking forward into the clinical portfolio, the dominant program that we'll spend a lot of time talking about today is our innovative GalNAc-conjugated INHBE siRNA program. We've been able to see a highly differentiated approach to treating obesity that's driven off of an improvement in body composition, meaning reduction in fat and muscle preservation. In addition to the groundbreaking work we've been doing in RNAi, we've been leading the field of RNA editing and pioneering that with our Alpha-1 antitrypsin program, and we'll share more data on that program later, as well as the advancement of the next program on our RNA editing platform, PNPLA3 for liver disease. Beyond what we've been doing with GalNAc conjugation for liver with siRNA and RNA editing, we've been able to advance an extrahepatic set of programs, both in RNA editing and in siRNA, delivering to adipose tissue, muscle, as well as CNS. And we'll share a little bit of data that we've built beyond our R&D Day on the novel bifunctional modality. And this really lets us think about taking these two opportunities in siRNA RNA editing into a single oligonucleotide construct that lets us have one drug that can both upregulate and edit, as well as silence a second target. So a lot happening, but a core focus that we'll share on obesity and Alpha-1 antitrypsin and editing. We're well capitalized, and we entered this year with now $602 million of cash, which will take us into the third quarter of 2028. So as we talk about our innovation on chemistry, and it is really important to take this as a foundation because as we think about this field, there's others in this approach who are talking about RNAi, and we need to think about how these approaches are different. Why is the chemistry different? So on the left-hand panel and on the far left, you'll see data that's represented from one of our papers that we shared several years ago. This was an NAR paper. And what we shared in the paper is that black line and that teal line. And when you look at the paper, what we showed is that the innovation that we see on our siRNA chemistry is giving us about a 10- to 15-fold improvement in AGO2 loading, yielding a more potent and durable knockdown in siRNA. What we've shared an update on at our R&D Day is that actually, with the innovations that we continue to push forward on our chemistries, that we're actually seeing much deeper knockdown. So again, enhanced AGO2 loading leading to deeper knockdown of the target, but even more durable suppression of that target. This is going to be critical as we talk about INHBE and the opportunity in obesity, where we can differentiate based on our siRNA formats between our chemistry and that of others that are moving forward. I should say that that black reference compound represents the state-of-the-art siRNA chemistry as it stands today. So we'll talk about this again in the context of obesity. In addition to the work that we're doing in siRNA, these chemistry innovations also apply to new modalities, so new modalities like RNA editing. And as we shared what we're able to do in highly potent, highly specific base editing, so this is A-to-I editing, we can see these chemistries transition to more potent, durable editing, and that translating ultimately into the portfolio. As we said at the beginning, while we've built a deep and broad portfolio of chemistry translating across programs in the clinic, across different modalities, 2026 is a year of strategic focus. When we talk about strategic focus, that really means an emphasis on two areas. The first area is accelerating the development plans for WVE-007 across multiple treatment settings within obesity and rapidly advancing our RNA editing portfolio of WVE-006 for AATD, as well as WVE-008 for PNPLA3. What does that mean? So in obesity, it means moving, as we announced yesterday, to the Phase 2a portion of the INLIGHT study. This is the multi-dose portion where we'll be exploring the ability to knock down INHBE in patients with higher BMI and with and without comorbidities, and we'll share more on that later. In addition, it also means that we're going to initiate new clinical studies in both a combo and add-on study to increase, as well as a maintenance. We think two very important opportunities to explore the 007 program. In RNA editing, it means delivering the data from the 400- and 600-milligram cohorts this year. The 400-milligram editing data for WVE-006 is coming this quarter, as well as filing the CTA and transitio ning WVE-008 for PNPLA3 for the nine million patients living with liver disease into the clinic. Looking forward to obesity, we do believe that obesity is in need of a treatment paradigm shift. We know that the current standard of care for GLP-1s is limited by a loss of muscle mass, and this is consequential, and we'll share more on that later, not just in the case of thinking about frailty, but really thinking of muscle as an endocrine organ. It's characterized by frequent dosing, poor tolerability, and discontinuation rates that are driven from that. When we think about the future of obesity therapy beyond incretin therapies, we're thinking about what the possibility is when you can improve body composition. WVE-007, to flash forward ahead, we saw fat loss similar to GLP-1s at the three-month time point. It preserves muscle mass, so very importantly, and we'll talk about the consequences of that. Preserving a muscle mass has the potential for once to twice-a-year dosing, both in the preclinical data as well as in our clinical data. Very importantly, for an obesity therapy, was generally safe and well tolerated, and we say that that was all the way through the 600-milligram dose cohort in the study. We believe that this principle of what we're bringing forward has the potential to change and improve body composition for the over one billion patients worldwide living with obesity. When we talk about body composition, there's often a, well, what does that mean? How important is body composition? We have to think about body composition as having two components. The first is a reduction in fat, in particular visceral fat, that's critical to when we think about cardiovascular outcomes, inflammation, MASH, and a number of diseases that are associated with obesity. Those are driven by increasing levels of abdominal visceral fat. INHBE silencing does reduce subcutaneous fat, and that's obviously important as we think about the majority of body fat, which is tied to body weight reduction. So we will see a reduction in fat as well as a reduction in abdominal visceral fat. Equally important is thinking about muscle preservation. We say this is important again beyond frailty because muscle is a very large endocrine organ that's responsible for improving insulin sensitivity. But as you maintain that and lose body weight, it is also a feature in how you can continue to progress body weight reduction over time. So preserving muscle is crucial in a therapy for obesity. So how do we think about INHBE? INHBE is a wonderful target in that it comes from the UK Biobank. So we like targets that have protective loss of function variants where essentially the human clinical trial has been run. This means that in the human population that's been studied in the UK Biobank, a 50% loss of function of INHBE has a genetic profile of low waist to hip ratio, so low abdominal visceral fat, has an improvement in lipid profiles, so low LDL, high HDL, and essentially the clinical outcome experiment has been run. Patients with a 50% reduction of INHBE have a low risk of type 2 diabetes as well as cardiovascular disease. So an ideal way to come into a program is one where the human experiment has been run, the genetics are there. The question that always comes forward is, can you induce a change in that phenotype? Well, how do we do that? So thinking about silencing INHBE, so this is a target that's produced in the liver, so an ideal target for a GalNAc siRNA construct. The liver target makes and forms a dimer of inhibin E, and that is the Activin E substrate. That is the protein of the ligand. We have assays that can measure activity in blood so that you actually have a great serum biomarker for efficacy, and you can measure the impact of silencing on that biomarker. Activin E binds to, and I'm sure people have heard of ALK7, is a receptor that's on the adipocytes, so the fat cell. So this is highly characterized communication of a hepatokine from the liver that cross-talks with receptors that are on the adipocytes. And if you silence that, so in a normal environment, let's say before we silence, Activin E binds to ALK7, and that's actually the body's mechanism for storing energy, storing fat. And evolutionarily, that's how humans protected themselves. You store fat, you store energy, and that protects you during times of famine. If you knock out Activin E, you remove the brakes on lipolysis from that receptor, and you see a shrinkage of adipocytes, fat cells, and it goes through lipolysis, and you lose fat. So that's the mechanism between the two. The efficiency and the reason we chose INHBE is the efficiency of taking a catalytic siRNA with GalNAc to a specific cell type that produces the ligand, the hepatocyte, and being able to turn off the spigot and prevent Activin E from engaging with the receptor is a highly efficient way to target this pathway. Now, there are other approaches of looking at Activin E in the periphery around the adipocytes. We do believe that targeting GalNAc to the hepatocyte is the most efficient way to drive this process. Now, this Activin E is in circulation, and recently there's been some discussions of whether or not type 2 diabetes has a role to play in weight loss with INHBE therapies and others. We'll say that a very large prospective, or I should say observational study in 250 patients was presented in a poster at Obesity Week. And in this study of 250 non-diabetic patients, it was seen that Activin E levels correlated with increase in BMI, increase in truncal and abdominal fat, and increasing in fasting insulin, all suggesting, similar to the data that we'll share soon in our healthy overweight population without type 2 diabetes, that type 2 diabetes is not connected with the INHBE Activin pathway in terms of weight loss, but actually BMI is highly correlated. And we'll talk about that in the context of moving into high BMI patients in the next study. What did we see preclinically that drove our enthusiasm around this target? It is that we did see that with our chemistry, being able to take a single dose and silence INHBE, it led to a potent, durable reduction of Activin E levels. That reduction of Activin E below our threshold of 70 caused a reduction in fat, particularly visceral fat, preserved muscle, and there was a slight increase in lean mass that we saw preclinically. We'll talk about that in the context of the human data, and ultimately resulted in body weight reduction in the DIO mouse at a similar level of weight reduction to GLP-1s. What you'll notice in that line on the far right, in terms of the INHBE weight loss curve versus the Semaglutide weight loss curve, is there's a shift in that rate of weight loss and weight decline. Originally, before our clinical data, it was thought that maybe lipolysis takes longer, and that might be accounting for that change in that slope, even though we reached the same standpoint, and that SEMA moves pretty rapidly. I think what we're seeing, both on our preclinical data and ultimately, as we'll share on our clinical data, is that rapid weight decline in Semaglutide is principally driven through a decline in loss of lean muscle mass. We'll share the 12-week data from the SEMA from the BELIEF study, but at the 12-week time point, it's actually about 50% in humans' lean mass loss at that early time point, and hence why we think the steepness of that curve moves pretty rapidly. What's interesting with INHBE is we actually see that this weight loss, while slower, is principally driven because you have stabilization of lean body mass and then continued reduction in subcutaneous fat, and that continuous reduction in subcutaneous fat drives weight loss, and so that's an important characteristic as we think about the profile as we move forward. Importantly, beyond monotherapy, so the idea that, you know, can you take down INHBE and does that drive weight loss similar to GLP-1s, we also saw the potential for combination. We've had a number of discussions with a variety of folks who've got lots of different programs across the incretin landscape of different ways to be thinking about how to drive this study as we think about our clinical study, but what was important is these approaches are completely orthogonal. The idea that INHBE and its pathway is non-calorically driven, and we'll talk about that in the next slide when we look at the caloric comparisons on the maintenance study. But given that you have an orthogonal approach of one being calorically driven or hedonically driven, which is the GLP-1 pathway, one that's driven on lipolysis and the pathway for INHBE, they are combinable and synergistic, and we can think about approaches of titrating between GLP-1s as well as INHBE to drive weight loss. Now, what's really exciting to think beyond the combination is the opportunity for maintenance. And so this study, which we ran, where we tracked both calories and weight, what we could see is as you induce on a GLP-1, you see weight loss very similar. You have that antihedonic behavior. Mice lose weight, both in the scope of lean muscle mass as well as in fat, and what we showed is if you predose prior to cessation of GLP-1s, you could curtail the rebound weight gain. This is independent from the fact that in both arms, the placebo arm and the treatment arm, caloric consumption resumed back above baseline, so essentially what happened is that starvation phenotype, now eating and storing calories, drove an increase in weight, all fat, but if you pretreat and took the brakes off lipolysis, you see a steady state of maintenance therapy, so these are the three treatment settings: mono, combo, and maintenance that we've been looking at for INHBE preclinical data. Transitioning to our clinical data, we ran a healthy overweight volunteer study. This is a Phase I study. The criteria, while the BMI, as you could see, had a larger range, the criteria that restricted that was that these had to be healthy patients, so no comorbidities, and in that, the average BMI on this study was 32, so substantially lower than that seen in other obesity trials. Additionally, there was no diet or exercise modifications required as part of this study, so this gave us a real-world setting where we could treat and see how patients actually low BMIs behaved on treatment. Cohort one, because this was a Phase I healthy volunteer study, was a subtherapeutic dose, and then the subsequent cohorts, 240, 400, and 600, were at or above the therapeutic expected threshold. I should say at the current time, all cohorts have been dosed. We've been cleared by the DSMB to go higher than 600, but as you'll see from the data, we don't believe that that's necessary, but it was important for us from a safety assessment when we did our first data cut that the safety assessment included all cohorts on the study, so what do we see? We saw a highly durable reduction in Activin E levels, and I think this was incredibly important when we think about it in comparison to other inhibin E programs that have been in development. We see in ED50 that's nearly threefold higher than other programs. So we're seeing potent, durable reduction of Activin E. Even at the subtherapeutic level, we're seeing that that's sustained out past six months, and we believe, looking at the 240 and the 400, that that should continue to support the once or twice-a-year dosing regimen. I will say that at the time of the data cut, the 400 is still going down, and we'll share that we'll expect that data this quarter where we'll have the follow-up data on the 400 milligram. But we see that we're in the threshold, it's stable, and it's durable. I'll also say that there's really good distribution into the hepatocytes. So if we look at the error bars between the six patients that were on the 400 at the time of the cut and the six patients that were in the 75 milligram, as we get that higher level of exposure, we're not concerned that there is lack of variability or distribution across patients. So again, highly encouraging as we think about the therapeutic profile continuing to mature. As we think about the clinical data, we saw much the recapitulation of that same data, so from human genetics to DIO mice, now to humans, with a substantial reduction in visceral fat, nearly 9.5%, a substantial reduction in total fat mass, and a slight increase above placebo in lean mass, again, consistent with what we saw in our preclinical data. When we take these data and compare them to the only now published data on 12 weeks with GLP-1s that include DEXA, so we can do points of comparison, we see that, and have to recognize that the semaglutide study at this point had a BMI of 36, so it's nice that we're comparing from a BMI of 32 with no diet and exercise to a study with a BMI of 36 with diet and exercise. But in that study, we still see substantially decreased abdominal visceral fat when we compare that to GLP-1. We see about equivalent reduction in total body fat, so again, similar body fat reduction to GLP-1s at that time point. But importantly, that slight increase in lean mass versus substantial decrease. And what's interesting there is we said earlier at that time point, there's about a 50% reduction in lean body mass. So again, very important that what we're seeing at this time point is fat reduction and importantly, visceral fat reduction, as well as retention of lean body mass. We do expect this study, as it continues over time, to continue to see, like we saw preclinically, continued sustained reduction in fat, preservation in muscle, and when you put those two parameters together, that should continue to drive reduction in total body weight. That's important because what we believe and continue to focus on is a regulatory pathway that follows the obesity guidance, which is a 12-month study looking at greater than 5% change in total body weight with an emphasis on body composition. So we do believe that these data continue to push in the direction of an obesity study driven off of fat loss with muscle sparing. One of the other things we can look beyond just generalized fat loss driving subQ and ultimately weight loss is the impact on visceral fat. And I think this is an important point of differentiation because what is seen is that a 7%-10% decrease in visceral fat ultimately can play a role in cardiovascular outcomes. So as these studies continue, the ability to think about not just the impact on body weight through a reduction in subcutaneous fat as the dominant reducer, but actually visceral fat should point to an improvement in cardiometabolic outcomes. So what's next for INLITE? Beyond the INLITE Phase I portion, which will continue to accrete over time, the study allows 12-month follow-up at each cohort, so we'll continue, as I said, all patients have been dosed, so we'll continue to follow these patients out over time. The goal as we announced yesterday is to accelerate the phase 2A portion, the multidose portion of the study. That's going to enable us to change the criteria to have higher BMI individuals, where we can then look, in addition to having comorbidities, we do expect a larger impact on fat reduction with higher BMI and therefore a bigger impact in overall changes, and then therefore can look at that in comparison with similar BMI studies that have been done. We plan to initiate this study in the first half of this year. Focus on that study being the monotherapy, so building on our single dose, we do see a monotherapy application for weight loss with a once to twice-a-year drug that loses fat and preserves muscle. We do see the ability, and we'll initiate this year the combination study to look at the add-on effect. And I think, as we've seen from other studies that have reported out recently, the power of the combination, particularly in liver fat reduction, has been pretty consequential. And so we see inhibin E in combination with incretin having a big impact on reduction of liver fat. So that's an important thesis to think about as we go forward. And then ultimately, where we see a very substantial portion and utilization of this is in maintenance, the idea that we can transition patients from a life of chronic incretin therapy to a once to twice-a-year maintenance drug. The key that's there is thinking about, as we think about the over a billion patients living worldwide with obesity, how can we move this beyond the United States and think about patients worldwide where you can get better access, better distribution if you only have to treat patients one to two times a year. So exciting. The value of this program continuing to go forward is now we'll continue to accrete data over time, and that data will really answer a question of how much does time play a role in continuation of body weight, how much is driven based on dose and Activin E reduction. This study is already poised to deliver on both of these features as we look at data over the course of this year. Beyond obesity, WVE-006, which is the first RNA editing program to go in the clinic, is moving forward. And a quick update on that, for those who aren't familiar, AATD, rare disease, focuses on about 200,000 patients in the US and Europe who have a ZZ mutation. So these patients have two bad copies of a gene. This creates a misfolded protein. That protein is unable to be expressed and protect the lung, and those patients go on to have lung injury. But also, because of that protein misfolding, go on to have liver injury due to the accumulation of that protein in the liver. There's no approved therapies that treat both the lung and liver manifestations of the disease. There is IV protein replacement therapy that's been approved to treat the lung conditions and to try to provide protein to protect that lung during periods of injury. There's no approved therapies yet to deplete the liver protein. The approach that we have is grounded in genetics, therefore looking at the heterozygous patients. These patients have 50% corrected M protein, so they are able to make a good copy of that protein. When you look at these patients, they have greater than 11 micromolar of protein that's able to circulate and protect the lung. They have 50% edited M protein. This is important because they're able to have a dynamic effect that can actually rise to meet that injury signal. These patients go on to have low risk of lung and liver injury. The principal guiding feature in developing the AATD program is developing a corrector that can correct over 50% of the transcript and therefore deliver the restoration of this healthy phenotype. The other key dynamic effect, and this is important as the data came out, is thinking about augmentation therapy, so this replacement versus correction. And I think what's interesting, and you have to reframe a thought of what happens to these patients. So what happens in the case of AATD patients is they have chronic disease, but there's acute exacerbation. So these patients go through these intervals where they'll have a stimulus of inflammation that drives an increased protein response of damage. And normally, these patients would make Alpha-1 antitrypsin protein to protect their organ, the lung. In the case of not having that, you get augmentation therapy. The challenge with augmentation therapy is you do this peak infusion, and then over time, as you can see on the graph, it's a consumptive protein, it declines. Actually, during that period of injury, patients are actually more exposed to that injury signal than they would be. Nobody knows kind of what happens in that interval as the protein's consumed, how much risk of injury there are, and it's a concern for clinicians. The difference of editing and correcting is actually the protein rises to meet the need of the body. You reach a steady state at that heterozygous level that protects the body. During that injury period where that stimulus is there, you actually see the increase in transcriptional activity and through correction can actually increase the expression of protein to protect an individual during that period of time, therefore preventing the exacerbation from driving injury. The current design of the study had a healthy volunteer component that's been completed. We reported data from the 200 single and multidose study last year. We shared the single dose data from the 400 last year, and the data this quarter will be from the 400 multidose cohort looking at M AAT levels, total AAT levels. What is important from the last time we reported data is exactly what one would expect or want to see in that heterozygous phenotype. We saw the lowest single dose of the study. We saw 13 micromolar of protein at a steady state. We could see the actual correction, and it was highly tight across patients in terms of that switch from Z protein to M protein, so we saw over 64, so well over 50% edited protein that could meet the need of that correction, and very importantly, we actually saw during the acute phase response, when the patient needs it, they could produce over 20 micromolar of protein, so a patient had an actual event during the study. We could look at the CRP level during the study, and it was a modest level, but we could actually see that they could generate over 20 micromolar of protein during the event. That's essentially where people are talking about where IV protein replacement should start before it actually starts to deplete. So when we think about the profile of delivering the heterozygous-like phenotype, we were seeing that at the early parts of the study. As we said, we'll have the 400 milligram data in Q1. Building off of this program, and very quickly, a lot of the principles of editing and can we get to this 50% editing, highly efficiency, GalNAc conjugated, subQ, a lot of the features that we'd like to see coupled with generally being safe and well tolerated was, could we apply this to another indication? There's often a question that gets asked, what are other large indications beyond alpha-1 antitrypsin? PNPLA3 is actually that mutation is a very interesting mutation. There's a strong foundation in human genetics. There's over 9 million patients that have in the U.S. and Europe that have this mutation, and it drives an increased incidence in liver disease. It's an enzyme, so it also has an approach where the 50% correction doesn't have this dynamic response event. So it's, how should I say, nothing's ever easy, but you can measure this and say that actually you're just measuring, can you correct this protein and allow it to restore its function? And the function really is about processing lipids as well as retinol, so be involved in fibrotic cascade. So when you think about that, given that it's involved in both lipid metabolism as well as fibrosis, you imagine that if you have that mutation, you can get a whole variety of liver diseases that come from this. So it's not restricted to MASH as an indication, although several companies talk about silencing in that approach. All told, liver disease for PNPLA3 is how we think about this. And with that mutation, you have about, and if you can correct that to the heterozygous level, you have about an 80% risk reduction of disease. So very similarly, 50% correction drives an improvement ultimately in outcomes. Why silence versus edit? It's been known that this is an enzyme that's really important, again, in lipid metabolism and fibrosis. So what we see in the control, the green high, the blue highlights are the nuclei of cells, the green is liver fat. And what you can see is if you can correct that protein and actually restore its physiologic function to 50% or more, you actually see better lipid traffic, and you metabolize that fat that's processed without the cell. We think this is why the siRNAs have had challenges, which is if you knock that enzyme out, you actually don't restore lipid metabolism, you don't restore retinol metabolism, you can see fibrosis. So we think it's an ideal target that's differentiated in the approach of why do editing and also attack a disease that's consequential. We see continued potent editing. We have the experience of translation from our preclinical models to clinical with alpha-1 antitrypsin. We see highly potent durable editing in our preclinical studies. Highly specific, and this is a good point of differentiation as we think about the DNA editing constructs, is that this editing is highly specific with no bystander edits, no off-target edits. We see really strong tissue distribution, delivery, and durability, and expect to file a CTA in 2026. Lastly, being able to put these two pieces together, we are working on bifunctional conjugates, where we actually take the best of what we can do in RNA editing, the best of what we can do in siRNA, and rather than making two molecules to drive therapeutics, can actually create a single oligonucleotide construct that can do both editing and upregulation coupled with silencing. I've shown data preclinically at our last research day that you can think about targets like LDLR upregulation with PCSK9 silencing and think about applications where you wouldn't want to have two independent development plans, two commercial products to be co-administered, but think about it as one clinical trial with one product to transition to the market. So the key focus for Wave going forward is an emphasis in RNAi driven by obesity with 007 for INHBE, 006 in AATD, and PNPLA3 with the ability to continue to drive those platforms and formats forward. Anticipated milestones, multiple data sets accruing on obesity over the course of this year, with the next inflection being Q1, the 400 milligram three-month data and the 240 milligram six-month data. Additionally, 006, first quarter, we'll have the 400 milligram data. 008 moves into the clinic. We do expect to submit the NDA for N531 this year. However, we've been very clear on our strategic focus that we will look to find commercial distribution partners for that as opposed to invest the capital that we currently have allocated for advancing our siRNA program, particularly running those three trials that we mentioned in obesity, that we'll use those partnerships to drive the N531 study forward, and with that, thank you for your time. Great. Great, thank you, Paul, for that presentation. So I thought I would just dive right in in the time that we had and start with obesity. Can you speak in a little bit more detail to the size and the scope of the Phase I additional INLIGHT trial data that we will get this year? What is the type of profile you're looking to deliver in this trial overall, and what level of fat loss and body composition results would you like to see with longer-term follow-up and higher doses? Yeah, we'll unpack that in a variety of ways. I think first and foremost, kind of stepping back to INHBE, INHBE right now has over 100 patients currently dosed in the study. So when we think about the magnitude of effect and being able to observe that over time, we have a substantial number of patients that we can look at across the study for both Activin E reduction and correlating that ultimately to therapeutic effects. So we do care about sample size and powering as we think about being able to identify impact and effects from the study. In terms of what we want to see is we'd expect to see continuation of what we currently see, meaning we saw that if we potently and durably reduce Activin E, it translates to a reduction in fat. Emphasis on visceral fat, but that's not to say that we don't see substantial reduction in subcutaneous fat, which should continue to drive the potential for weight loss as well. So we see fat reduction, and we see lean mass preservation. The profile that we'd expect to continue over time, both at that dose, and then we'll talk about what happens as we go higher, is that we would expect to see fat continue to decrease, but we would expect lean mass to stay stable. And so again, when we think about what would drive the ultimate, this is kind of the calculation for how to think about body weight reduction, is that if you change body composition and that reduction in fat and you keep lean mass stable, you will lose body weight. I think the important observational medicine to see that, and it was in the BELIEF study, is Bimagrumab, so a totally different pathway that's a myostatin medicine that makes lean mass go higher and actually has less an impact on fat, still sees weight loss over time. Again, we expect that profile of focus on fat reduction, lean mass sparing to drive that. I think what we're going to have the opportunity with this quarter is to see the impact of dose on the rate of change. Does a higher dose actually drive that transition faster? Ultimately, does it allow that to continue out longer? We'll be able to look at both dose response as well as time response on body composition as the study continues to progress. Then the opportunity with the higher BMI Phase II A portion is going to be able to see the impact of higher BMI on that rate of change. Great. And you talked a little bit about the number of different treatment settings you could go into here. How do you think about overall Phase II development, and which of the pathways do you think are most de-risked at this point versus where there may be a little bit more risk? De-risking has two different components to it. I think on one hand, we do see on the monotherapy side a de-risking event that substantial reduction of Activin E causes substantial reduction in fat, which is tied mechanistically to both the animal model where we saw fat reduction similar to weight reduction similar to GLP-1, as well as the human clinical genetics. I think on the other side of the equation beyond monotherapy is actually there's substantial data on maintenance because if we think about the human heterozygous phenotype, there's a lifetime of maintenance essentially with a 50% reduction in the genotype that ultimately leads to an improved phenotype over time on maintenance therapy of what happens when you reduce Activin E, those patients don't gain weight. So when we think about the maintenance setting where a person's at a set body weight from an incretin and you're dosing and withdrawing the incretin, that's probably the most correlative to when we think about the human clinical genetics, but we'll be running that study as well. Any further comments you want to make on kind of overall where you see this asset fitting into the treatment paradigm here and also just how you see the evolving development landscape in the kind of the area that you're in? Yeah, there's a lot to discuss there. I think in each treatment setting, we see high need and impact. And if we work from the maintenance setting forward, I think in maintenance, keeping patients on a lifetime of a multi-dose incretin therapy has challenges. And I think we hear that from a number of individuals we talk to, clinicians, patients, even strategic partners thinking about how do you continue to keep patients on incretins for a very long period of time. I think one approach that has been suggested is why we see the shift to oral medicines, but as we've learned from the statin community, trying to stay on an oral daily statin that actually has very low incidence of side effects is very hard to do consistently, and compliance is a very difficult problem in keeping patients on therapy. Flash forward to an oral medicine that drives nausea, vomiting, and my guess is that real-world data as it emerges, we'll see how that continues to drive a maintenance therapy. So I think the idea of rapidly transitioning patients to a once to twice a year therapy that allows for sustained fat reduction, preservation of lean mass, and has a safety tolerability profile as we do, I think is an ideal way of thinking long-term about that opportunity. And we know what the current opportunity sits with that transitioning of those patients forward. Combination is real. We know patients who come in and talk about their journey with us and remind us that they could be looking at an advertisement on television that shows what the weight loss opportunity is in combination and says even if they achieve that, they still wouldn't be at a treatment goal of healthy weight loss, and so therefore, the additional setting of being able to add this on to existing incretins to continue that weight loss journey is important because, again, because of the safety tolerability profile, the combination actually is not adding additional safety or tolerability events. We also have seen and had a number of strategic discussions about how do we think about these interacting in terms of titrating back incretins and finding an optimized schedule between incretin therapy along with a combination, so that's intriguing, and I think there's a number of different ways to explore that. And then we're working our way back to monotherapy. And I think this is one of what is that rate of weight loss. And I think when people can have the conversation move from this being a pound-for-pound weight of weight reduction, which is principally driven off of lean mass, and I don't know many people saying, "I want to lose like 50% of my lean mass within three months if given an opportunity," the opportunity to reimagine what that looks like when you can have a monotherapy that you preserve your lean mass, you lose fat, weight loss will occur, but in terms of improved body composition, we think that is ideal. As we talk to clinicians who are saying, "Look, I've got patients who I'll tell them they've got to eat protein, but the anhedonic activity of the GLP-1s is having them not consume the protein that they need to retain that muscle," I think the treatment paradigm in monotherapy is ripe for migration. But we realize that that will take time for the community to adapt. And so I think all three treatment settings are an opportunity. Okay, and I know it's such a tight amount of time here, so I'll just ask kind of an overall question to end us. Are there any other data milestones that you think matter most for Wave in 2026 that you would draw people's attention to? I think the upcoming data is we think about the continuation of 007 and driving improved body composition. Again, as a paradigm-shifting is probably the most watched, the most focused on opportunity, and the benefit we have is as we roll forward, we're going to have ample opportunities to see that data continue to accrete both at each dose level over time, but also at the higher doses to see the continued improvement in body weight reduction. Okay. Okay, great. Thank you so much, Paul, and the entire Wave team. Thank you. Thank you.