Joining me today are Andrew Cheng, President and CEO of Akero, Kitty Yale, Chief Development Officer, and Tim Rolph, Chief Scientific Officer. Today, we will be sharing 24-week top-line results from our ongoing HARMONY Phase 2b clinical study of efruxifermin or EFX for the treatment of NASH. Before we begin, I ask that you please read the disclaimers presented on slide 2, and I'd like to remind you that various statements that we make during this call will include forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including express or implied statements regarding implications of this analysis of the HARMONY study, our future plans, including our plans around the development of EFX, prospects and strategy, financial goals and guidance, product attributes and pipeline, drivers of growth, and other statements that are not historical facts. Such forward-looking statements are not guarantees of future performance, and therefore you should not put undue reliance upon them. Management assumptions, expectations, and opinions reflected in these forward-looking statements are subject to risks and uncertainties that may cause actual results and/or performance to differ materially from any future results, performance, or achievements discussed in or implied by such forward-looking statements, and the Company can give no assurances that they will prove to be correct and will not provide any further guidance or updates on our performance during the quarter, unless we do so in a public forum. Please refer to the press release we issued this morning and risk factors included in the Company's filings with the Securities and Exchange Commission for a discussion of important factors that may cause actual events or results to differ materially from those contained in our forward-looking statements. Prior to this call, we issued a press release regarding data from our Phase 2b HARMONY study, which is available on our website at akerotx.com under Press Releases in the Investor Relations section. The presentation we'll walk through on today's call will be available immediately afterwards under Events and Presentations in the Investor Relations section of our website. I will now turn the call over to Andrew Cheng, Akero's President and CEO. Thank you, Bill, and thanks to all who have joined today's webcast. Today, I am very pleased to announce exciting new data from our phase 2b HARMONY study of EFX, the Fc-FGF21 fusion protein we are developing as a treatment for non-alcoholic steatohepatitis, or NASH. Both doses of EFX administered in the study achieved statistically significant improvements on each of the two main histological endpoints that regulators have stated will be acceptable to support an application for registration, as well as a composite of both endpoints. The level of efficacy based on these histological improvements strengthens our belief that EFX will ultimately be approved as a medicine for NASH. Moreover, because it also improves whole body metabolism, which is the key to sustainably improving liver health, we believe EFX will be a potentially foundational treatment for advanced fibrosis due to NASH. We set high expectations for EFX in the 24-week HARMONY study based on the promising results observed in the 16-week Phase 2a BALANCED study. The data we report today have met and exceeded those expectations and contribute to a growing body of data that shows EFX has what it takes to treat the core facets of NASH. We believe today's compelling results are an important milestone, not only for Akero, but the entire NASH community. As a leading cause of liver transplantation and liver cancer, and a major cause of cardiovascular mortality, NASH represents a substantial and growing health burden. We believe the data are unambiguous in showing EFX's potential to address this critical unmet need, particularly for patients with advanced fibrosis. I'll now have our Chief Development Officer, Kitty Yale, dive into more detail on today's data. Thank you, Andrew, and good morning, everybody. I'm thrilled to report the 24-week results from the HARMONY study. We are especially pleased with the consistently large magnitude of observed effects across all endpoints and the statistically significant results. Importantly, the HARMONY results were generally consistent with the results of our previous Phase 2a BALANCED study. The safety and tolerability profile was also in line with expectations, with no new safety signals of concern observed. Bottom line, we're excited about the strength of these data and the foundation it provides for potentially favorable results in our ongoing Phase 2b SYMMETRY study in patients with cirrhotic NASH. I'd like to begin with a review of the design of the HARMONY study, which is shown on slide 4. The HARMONY study is a Phase 2b randomized, double-blind, placebo-controlled, multicenter dose-ranging trial in adult patients with biopsy-confirmed NASH. The HARMONY study was limited to patients with biopsy-confirmed fibrosis stage 2 or 3. Patients were randomized to receive once-weekly subcutaneous doses of either 28 mg or 50 mgs of EFX or placebo. The primary endpoint was the proportion of subjects who achieve at least a 1-stage improvement in fibrosis without worsening of NASH at week 24. Secondary measures include NASH resolution without worsening of fibrosis, change from baseline in liver fat, liver enzyme, non-invasive markers of fibrosis, glycemic control, lipoproteins, and body weight at week 24. As well as safety and tolerability. We set a high bar for success when designing the HARMONY study. It was designed around the two histological endpoints that need to be met in a future phase 3 study for marketing approval in the U.S. and Europe. These are 1, fibrosis improvement of at least one stage without worsening of NASH, which is the HARMONY study primary endpoint, and 2, NASH resolution without worsening of fibrosis. According to FDA draft guidance in developing investigational drugs for pre-cirrhotic NASH, FDA will accept either one of these two endpoints for marketing approval. In Europe, by contrast, the EMA requires both endpoints to be met. Accordingly, succeeding on both endpoints is a prerequisite for developing a truly global therapeutic. Let's review how we got to the group sizes for the primary endpoint statistical analysis and the other data set. As shown on Slide 5, 128 patients were randomized. 2 patients were randomized but not dosed. 11 of the 126 dosed patients, or about 9%, discontinued prior to week 24. In HARMONY, six of the eleven discontinuations were described as being seen for administrative reasons. The remaining five patients discontinued due to adverse events, two in the 28 mg group and three in the 50. Of the remaining 115 patients who completed week 24, two patients declined to be biopsied for a second time. Consequently, 113 patients are in the liver biopsy analysis set used for all histological endpoints, including the primary endpoint. There were 41, 38, and 34 patients for the placebo, 28 mg, and 50 mg EFX doses, respectively. On Slide 6, we review the baseline demographics. These baseline measures are generally comparable to those observed in the biopsy-confirmed NASH patient population and similar to those in the BALANCED study. However, patients in HARMONY exhibited characteristics of more advanced stage disease. More than two-thirds of patients had type 2 diabetes, and two-thirds had stage 3 fibrosis. To ensure distribution across treatment groups, patients were stratified by these two parameters prior to randomization. The advanced stage of disease, with its negative impact on quality of life, was evident in the medical history of HARMONY patients. More than half of the patients were treated for mental health, especially anxiety and depression, often associated with chronic musculoskeletal pain and gastrointestinal dysfunction. As a result, over half the patients were taking multiple medications, in most cases on top of treatments for diabetes, hypertension, and/or hyperlipidemia. This complex polypharmacy increases the potential frequency of drug-drug interactions, making treatment of NASH with small molecule therapeutics challenging, a risk which we believe is significantly reduced for EFX as a biologic. Before diving into the histology results, it's important to highlight the new approach to biopsy analysis that was used for HARMONY, which is reviewed on Slide 7. Biopsy endpoints are prone to variability because they sample only a fraction of a percent of the liver. There can be differences in interpretation of biopsies from pathologist to pathologist and even by a single pathologist on repeat scoring. Most Phase 2 NASH studies to date, including our Phase 2a BALANCED study, have used a single pathologist to read biopsies. The FDA recently recommended a consensus approach to biopsy reading, which we expect to become the standard for NASH trials. Our consensus approach in the HARMONY study was to have all biopsies read by two well-trained pathologists. Each pathologist scored every individual biopsy sample independently. Our pathologists were blinded to subject and treatment assignment. Biopsies were shuffled to ensure the pathologists were also blind to visit sequence. If the scoring differed between the two pathologists, they conferred to reach a consensus. Our protocol specified that if consensus couldn't be reached, a third well-trained pathologist would adjudicate between the scores. However, adjudication was never required in HARMONY. Turning to our compelling efficacy data on Slide 8, we report the results for the primary endpoint of fibrosis improvement of 1 or more stages without worsening of NASH, which, to remind you, is one of the two accepted NASH histology endpoints for use in phase 3 registrational trials. Both EFX groups met the primary endpoint with 41% for the 50 mg dose group and 39% for the 28 mg dose group, compared to a 20% placebo response rate. Importantly, both EFX groups roughly doubled the placebo response rate after only 24 weeks of treatment. A reversal of at least one stage of fibrosis, which by definition includes people who experience a two-stage improvement, is expected to improve long-term clinical outcomes. Slide 9 places EFX fibrosis improvement in the competitive landscape. Relevant competitors have been arranged from left to right by reported magnitude of fibrosis response. Information relevant to how to interpret each data set is provided above the corresponding histograms. These differences in trial designs, patient populations, and other factors make cross-trial comparisons challenging, and no head-to-head trials comparing these various investigational drugs have been conducted. The effect sizes, meaning the difference between treatment and placebo for both doses of EFX, are the largest among those shown here. To our knowledge, this is the first report of a study with two treatment groups achieving statistical significance on the fibrosis endpoint. Slide 10 reports results for the percentage of patients who achieved NASH resolution with no worsening of fibrosis. The second accepted phase 3 endpoint. Both EFX treatment groups achieved statistical significance with high levels of NASH resolution compared to placebo. 76% of the 50-mg group and 48% of the 28-mg group achieved NASH resolution with no worsening of fibrosis. These response rates are respectively 5x and 3x the 15% placebo rate. Slide 11 places the NASH resolution rates in the competitive landscape. Relevant competitors are arranged from left to right by reported magnitude of NASH resolution and no worsening of NASH. Beginning with the 62% and 32% placebo-adjusted effect sizes for the EFX and 28-mg dose groups respectively. As you can see here, although cross-trial comparisons have inherent limitations, the effect size for the 50-mg EFX group is markedly higher than the next highest effect size shown, and more than twice, sorry, the size of the rest. Meeting each of these endpoints with statistical significance for both EFX groups is an important milestone for a phase 2 study, given the European requirement to meet both endpoints in phase 3. On slide 12, we review two additional endpoints that in different ways show how EFX had impressive results on higher thresholds for histological improvement. On the left, we show the percent of patients in each group who achieved both fibrosis improvement of at least one stage and NASH resolution at the same time. 41% and 29% of the 50 mg and 28 mg EFX groups respectively achieved both endpoints, representing 8- and 6-fold higher responses relative to placebo value of 5%. The size of effect at 50 mgs gives us confidence that EFX has the potential to demonstrate a safety and efficacy effectiveness profile that could support approval as a global therapeutic. As shown on the right, we also examined the proportions of patients achieving a 2-stage improvement in fibrosis without worsening of NASH. This endpoint represents a more stringent assessment of the standard fibrosis improvement endpoint, requiring at least a 1-stage improvement. Here, at least 15% of patients in each EFX group achieved this higher threshold endpoint, compared with 5% for the placebo arm. It's important to underscore the 24-week treatment duration used for the HARMONY study. Demonstrating significant reversal of fibrosis after only 24 weeks of treatment differentiates EFX from therapies aimed at reducing body weight, which take much longer based on published long-term follow-up of patients who lost more than 10% of body weight per year. We believe demonstrating histological improvements in fibrosis in a relatively short period of time, coupled with a higher rate of NASH resolution, has the potential to lead to rapid adoption as a therapy for NASH if approved. On the more immediate horizon, we are encouraged by the strength of our histology results and what they mean for our ongoing Phase 2b SYMMETRY study in patients with cirrhotic NASH. Based on today's results, we believe EFX has the potential to be the first investigational NASH drug to achieve statistically significant histological improvement in patients with cirrhotic NASH. EFX favorable histopathology results in the HARMONY study are underpinned by large improvements in markers of liver health, particularly normalization of liver fat content to less than 5%. Slide 13 shows the substantial reductions in liver fat content for both doses of EFX associated with normalization in one-half and one-third of patients treated with 50 mg and 28 mg, respectively, compared to 2% for placebo. Reducing liver fat is essential to removing the underlying drivers of NASH. These drivers include lipotoxicity, oxidative stress, and damage to intracellular proteins, resulting in endoplasmic reticulum stress, activation of cell death pathways, and ultimately inflammation and fibrosis. The beneficial impact on liver health arising from EFX substantial reduction in fat content is illustrated in slide 14, which shows that EFX rapidly and sustainably lowered serum ALT and AST clinical markers of liver injury. Statistically significant reductions for both EFX groups were observed at all time points from week 4 through week 24, reflecting EFX rapid and direct alleviation of liver cell stress. At week 24, there were dose-related reductions in ALT of 38%-47% for the EFX group, compared with a 4% reduction for placebo. For AST, we see similar statistically significant rapid and sustained dose-related reductions from week 4 through 24. Relative to baseline ALT and AST values, the roughly 40%-50% reductions mean that EFX restored healthy levels of liver enzymes during the treatment period for most patients. These improvements underpin the large improvements in NASH resolution after only 24 weeks of treatment with EFX. Slide 15 shows the effect of EFX on non-invasive markers of liver fibrosis, which present complementary measures of whole liver fibrosis. On the left, we report change from baseline for the serum biomarker of synthesis of new soft tissue collagen, Pro-C3, indicative of fibrogenesis in the liver. Here we see statistically significant reductions of 5.1-5.2 micrograms per liter across the EFX groups, compared with a 0.1 microgram per liter increase in Pro-C3 for placebo. This translates to reductions well above the 20% reduction that has previously correlated with a greater than one-stage improvement in fibrosis. The middle chart reports change from baseline in enhanced liver fibrosis, or ELF score, derived using an algorithm based on three serum biomarkers indicative of rates of soft tissue extracellular matrix deposition and turnover. The ELF score has been shown to correlate with stage of liver fibrosis and cirrhosis. Here we see statistically significant reductions of 0.6 and 0.7 across the EFX group compared to a 0.1 increase for placebo. A reduction of 0.5 has been reported to correlate with a one-stage improvement in fibrosis. The chart on the right reports change from baseline for liver stiffness measured by transient elastography using FibroScan. Here we see reductions of 2.6-4.3 kilopascals across the EFX groups, or roughly 15%-25%, compared with a 0.7 kilopascals decrease for placebo. In prior phase 3 studies of reduction in stiffness of greater than 25% was associated with fibrosis regression. Taken together, the statistically significant results on both biopsy-based endpoints and non-invasive measures of whole liver fibrosis and liver injury suggest that EFX has the potential to reverse fibrosis progression for patients with NASH and improve liver health. Let's now shift to safety and tolerability summarized on slide 16. Starting at the top of the table here, there were no deaths on the study. Only a single patient was reported to have a drug-related serious adverse event, or SAE. This patient from the 50-mg EFX group experienced a SAE of esophagitis. Notably, this patient had a history of gastroesophageal reflux disease. 3 patients had SAEs that were unrelated to EFX treatments. 1 patient experienced facial edema in the cheeks and eyes, which resolved with antihistamine therapy. One patient was hospitalized with COVID-19 symptoms. A third patient experienced pancreatitis. This patient was obese, diabetic, and had hypertriglyceridemia and severe insulin resistance at baseline, as well as a history of tobacco use, all of which increase the risk of pancreatitis, contributing to the investigator's assessment that it was not a treatment-related event. A total of five patients treated with EFX were discontinued due to adverse events or AEs. Two in the 28 mg group and three in the 50 mg group. One of the discontinuations in the 50 mg group was unrelated to study drug. In the 28 mg group, one patient discontinued due to diarrhea and another due to increased appetite and weight gain. As Tim will review shortly, while one patient discontinued due to increased appetite and weight gain, we observed an average weight reduction amongst EFX-treated patients. In the 50 mg group, 1 drug-related discontinuation was the patient who experienced esophagitis, for whom vomiting was also cited as a reason for discontinuation. Another patient discontinued due to nausea. The third patient discontinued due to lymphadenopathy, which was unrelated to treatment. The bottom portion of the table presents an overview of the drug-related treatment-emergent adverse events. Consistent with previous evaluations of EFX, the most frequently reported adverse events were transient, mild to moderate gastrointestinal events. The majority of GI events were grade 1 that either resolved on study or were easily managed during the study. There were very few discontinuations due to GI events. The majority of injection site reactions were grade 1 and had a similar incidence rate with placebo, and there were no discontinuations due to injection site reaction. I'd now like to turn the presentation over to our Chief Scientific Officer, Tim Rolph, who will present our biomarker data. Thank you, Kitty, and good morning, everyone. The sustained improvements we observed in liver health are underpinned by restoration of healthy metabolism at a whole body level, which we review starting with slide 17. This is critical for patients whose diabetes results in their liver being overloaded with energy, because the underlying resistance to insulin means peripheral fat depots and muscle are less able to take up glucose and fat. As seen here, control of blood glucose improves significantly, as indicated by a reduction of 0.5% in hemoglobin A1c for those patients with type 2 diabetes. Improved sensitivity to insulin generally reduces demand for secretion by the pancreas. Statistically significant reductions of 17% and 22% in serum C-peptide level for the 28-mg and 50-mg doses respectively, compared with a 16% increase for placebo, show a reduced rate of insulin secretion in those diabetic patients. We believe these data show EFX's potential to restore insulin sensitivity, enabling glucose, fat, and amino acids to be redirected away from the liver. In turn, taking pressure off the insulin-secreting pancreatic cells, protecting them from exhaustion and death. To put the clinical benefit of this in context, approximately two-thirds to three-quarters of patients in the HARMONY study dose groups had type 2 diabetes. Improving insulin sensitivity is highly desirable for this population because it delays progression to potentially requiring injectable insulin. Healthy whole body metabolism also requires restoration of a normal lipoprotein profile. Slide 18 shows change from baseline for serum levels of triglycerides and bad cholesterol, as indicated by LDL cholesterol and non-HDL cholesterol, which fell significantly after EFX treatment for 24 weeks compared to placebo. In the first panel, triglycerides reduced by 25%-29% across EFX groups, compared to an increase of 9% for placebo. Moving to the next panel, statistically significant reductions were observed for LDL cholesterol of 8% in both EFX treatment groups. Compared to an increase of 9% for placebo and 13% reductions for non-HDL cholesterol compared to an increase of 8% for placebo. On the other hand, levels of good cholesterol increase. Moving to the last panel, serum HDL cholesterol increased by 24%-30% across the EFX groups, compared to a 2% decrease for placebo. To put the clinical benefit of the improved lipoprotein profile in context, up to 80% of NASH subjects are dyslipidemic. Dyslipidemia is a major risk factor for cardiovascular disease, including heart attack and stroke, which is the major cause of premature mortality among the NASH population. Slide 19 shows body weight change after 24 weeks treatment. We observed significant reductions in weight of 2.6% for the 50 mg treatment group, while 28 mg of efruxifermin and placebo were unchanged. We continue to view the weight loss observed with EFX 50 mg as a potential key element of differentiation, with the potential for weight loss likely to be attractive to NASH patients and clinicians. Although statistically significant, we believe the weight loss at 50 mg is unlikely to account for the observed improvements of NASH-related histopathology. After accounting for modest differences in baseline levels, these very encouraging metabolic data are generally consistent with the results observed in the Phase 2a BALANCED study, in which patients were treated with EFX for up to 16 weeks. The two studies demonstrate EFX is addressing each aspect of the metabolic dysfunction associated with NASH by improving glycemic control through enhancing insulin sensitivity, restoring a healthy lipoprotein profile and lowering body weight. These broadly based observed improvements increase our confidence that the rapid reduction of steatohepatitis and collagen deposition seen in HARMONY will be sustained during the study's follow-up period with longer-term treatment with EFX. In turn, allowing further resolution of fibrosis beyond the highly encouraging improvements evident after only 24 weeks of treatment. In conclusion, we believe the breadth of desirable effects elicited by EFX to date in HARMONY and prior studies sets it apart from other candidates or therapeutic mechanisms in development for NASH, which, based on available data, can make lipoprotein profiles worse, increase body weight, and fail to improve glycemic control. I'll now hand the presentation back to Andrew. Thank you, Tim. The remarkable HARMONY data Kitty and Tim presented this morning demonstrates EFX's potential to address all of the core aspects of NASH pathogenesis in a single treatment. That is, reversing fibrosis, resolving NASH, improving liver health, and restoring healthy metabolism to the whole body. EFX's statistically significant results on primary and secondary histology endpoints represent some of the largest effect sizes reported to date. Both dose groups met the primary endpoint of fibrosis improvement without worsening of NASH at roughly double the 20% placebo rate. An unprecedented 76% of patients in the 50 mg dose group achieved NASH resolution without worsening of fibrosis, a response rate five times the size of the placebo rate. In addition to achieving statistically significant improvements on each of the two main histological endpoints accepted for phase 3 registration, HARMONY also delivered on higher thresholds with both doses achieving numerically 6x-8x the placebo response rate for the combined efficacy of fibrosis improvement and NASH resolution. The combination of these results with statistically significant improvements in liver health and whole body metabolism, including non-invasive tests of whole liver fibrosis, measures of liver stress, hemoglobin A1c, triglycerides, and importantly, LDL cholesterol, all within 24 weeks of treatment, strengthens our confidence that we may continue to see favorable results in our ongoing phase 2b SYMMETRY study in patients with cirrhotic NASH, which we expect to read out next year. We believe EFX has unique potential to address the diverse drivers of NASH and become a foundational monotherapy, particularly for patients with advanced stage fibrosis who typically have a worse prognosis and higher mortality rate than those with less advanced fibrosis. We look forward to working with the FDA and EMA to design our registrational development program and ultimately, if approved, to make an exciting, much-needed new treatment available to patients around the world. Before closing, I'd like to take a moment to extend our deep gratitude to all of the investigators, study site staff, and patients who participated in the HARMONY study. Today's exciting data would not have been possible were it not for the dedication of our investigators, their teams, and most importantly, the patients who participated. I'd like to turn things over to the operator for questions and answers. Thank you. Ladies and gentlemen, if you'd like to ask a question at this time, you will need to press star one. Please stand by while we compile the Q&A roster. Now, first question coming from the line of Michael Yee with Jefferies. Your line is open. Hi, good morning. This is Dennis from Mike. Congrats on the strong data today. It really looks very interesting, really good. Two questions for us. When we look across the NASH landscape, can you just help frame what you saw in the Phase 2b with what others have shown? I know you had a slide on this, but I'd really love to hear a little bit more. Number two, can you tell us a little bit more about, you know, the phase 3 and the path forward? When will you start that? Perhaps talk more about the trial design and what are some of the levers that you can pull to increase the probability of success? Thank you. Thank you, Dennis. It's Andrew. I would say when we look across those two landscape slides and look at the histology results in total, we have a unique package when one thinks about a compound that has the effect size that we have seen in both, fibrosis improvement, NASH resolution, and even the composite endpoint. I'm unaware of any other compound that really has that level of effect size across all three of those endpoints which have been used in registration. I think we're very pleased to have shown that in this study. Now, when it comes to next steps in our phase 3 development plan, let me turn that over to Kitty and perhaps give a higher level response to your question. Thank you. In terms of our phase 3 program, we're actually designing a 3-study program. We've initiated discussions with the regulators already around that program. Really, in terms of next steps, it's really finalizing the design of the studies in that program and getting alignment with both the FDA and the EMA. Those will really occur through sort of end-of-phase 2 meetings. Really for us, that's the next step, and it's sort of full steam ahead, you know, and finalizing those designs, getting aligned with the agency so that we can get into our phase 3 program as early as we can next year. Thank you. One moment for our next question. Our next question coming from the line of Eric Joseph with J.P. Morgan. Your line is open. Hi, good morning. Let me add my congrats on these data, and thanks for taking the questions. I guess first, in contrast to BALANCED, the data today would suggest that you're seeing a bit more of a dose response from 28 mg to 50 mgs. I'm just wondering from a tolerability standpoint, is it your view that the tolerability is essentially equivalent between the doses? I'm just trying to get a sense of what dose level you might advance in the pivotal program and how you might accommodate for any need for dose modification. Then secondly, sorry if I missed it in the baseline parameters, but can you just comment on background GLP-1 use in the study, at what rate and how well balanced it is across study arms? Sure. Eric, why don't we start with the GLP-1 percentage? It's roughly 15% in the study. In terms of how well balanced it is across the group, let me get back to you on that. I think it's not something that's top of mind for me right now. In terms of you know, the AE percentages, I think overall that the differences, as you pointed out, are a little bit closer between the two groups. When we think about selecting our dose of phase three, I would think that we have to look at the totality of the data. We actually. These data are really the top-line data. There's some individual patient data that we're still awaiting, so I think that will help us as we move forward. Maybe just one final. Sure. A question related to histology. Just sort of more of a housekeeping point. Any trend or imbalance as it relates to either NASH worsening or fibrosis worsening across study arms? Kitty, do you wanna take that? Eric Joseph, as Andrew Cheng said, these are still top line datasets, so we haven't got our entire dataset. What I would imagine that would be a presentation that we'll provide at a scientific conference at a future point, but we can't really comment on that right now. Okay, great. Thanks for taking the questions, and congrats again. Thank you. Our next question coming from the line of Ed Nash from Canaccord Genuity. Your line is open. Hi, thanks for taking my call. Just wanted to ask how would the stats change for an ITT analysis? And also, how would you expect the FDA to require an ITT analysis for data? Sure, Ed, it's Andrew. What I would say is that the Phase 2b study, as you saw from some of our landscape slides, most of the Phase 2b trials have used sort of a liver biopsy analysis set as the primary endpoint. I think the semaglutide study is the one that didn't, and they used an ITT analysis. The Intercept's results on our slide were phase 3 results. Their Phase 2b, which was the FLINT study, used the same sort of liver biopsy subset. That being said, to answer your questions, how the results would change when one looks at the histology endpoints of NASH resolution and one stage improvement of fibrosis, the percentages would come down in an ITT percentage, but they would remain statistically significant for three of the four. I think we lose the 50 mg at an ITT basis, and you can see why that makes sense given the slightly higher number of dropouts in that. Got it, okay. My last question is just with patients that have a greater than 2-stage fibrosis improvement? Mm-hmm. there was the 50 mg group was lower than the 28 mg group. Any reasoning there on why that's the case? I think it was just a little bit. I think it was 15 versus 16%. I think for us, numerically, we sort of see that as the same. Got it. Okay. Great, and really congratulations on that. Really impressive. Oh, thank you. Thank you. We have time for one more question. One moment for our next question. Our next question coming from the line of Ed Arce from H.C. Wainwright. Your line is open. Great. Thanks for taking my questions, and let me add my congratulations on really impressive data across the board. Two for me. Firstly, given these robust results, across both the histologic endpoints and broadly across multiple supportive endpoints, how do you believe physicians are likely to position EFX treatment relative to potential oral options? The second question, I was just curious, if you have any thoughts on why the placebo response in NASH resolution of 20% is larger than that of fibrosis improvement at 15%. Thanks so much. Yeah. Hi, Ed. I think in terms of when we think about this or how this gets positioned with physicians, I think we have to see that the totality of what the compound offers remains very attractive. When one thinks about a compound that offers not only improvements on histology for NASH resolution and fibrosis, but also for the other things that afflict these patients. When one thinks of weight loss or hemoglobin A1c control and lipids improvement, I think it's very attractive. It's a pretty attractive package. Now, obviously, it's an injectable, and so there's a bar there that is not insignificant. At the same time, when we look at how successful the GLP-1s have been as weekly injectables, it gives us an idea for such a huge market that, there's likely to be a good place for EFX to coexist with orals. Then you asked a question of placebo, when it comes to liver biopsies. I think, we would still say this is a small sample size. As Kitty mentioned in her presentation, liver biopsy has some degree of variability, and truthfully, I don't have a good answer of why the placebo response rate is slightly different, when one thinks about 20 versus 15 when it comes to those parameters. I think, for the sort of uncertainty of liver biopsies, those are relatively close numbers for us. Right. Got it. Great. Congratulations again. Thank you. Good to speak with you. Likewise. Now I'm showing no further questions at this time. We thank you for your participation, and you may now disconnect.