Good morning, ladies and gentlemen, and welcome to Akero's 36-week analysis of Akero's 96-week Phase 2b SYMMETRY study. As a reminder, today's conference call is being recorded. I would like to turn the call over to Bill White, Akero's Chief Financial Officer and Head of Corporate Development. You may begin. Before we begin, I ask that you please read the disclaimers presented on slide 2. 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. The Phase 2b SYMMETRY study of efruxifermin or EFX, our future plans, including our plans around the development of EFX, prospects and strategy, financial roles and guidance, product attributes and pipeline, drivers of growth, and other statements that are not historical fact. Such forward-looking statements are not guarantees of future performance, and therefore you should not put undue reliance upon them. Management's 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. The Company can give no assurance 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 the 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 SYMMETRY 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. Today, I am pleased to introduce new data from our Phase 2B SYMMETRY study of EFX, an Fc-FGF21 fusion protein we are developing as a treatment for NASH, including patients with liver cirrhosis due to NASH. Although obviously disappointed that the week 36 primary endpoint of fibrosis improvement was missed, we are encouraged by the totality of today's data and believe it supports moving EFX forward into Phase 3 in the cirrhotic population. In the trial, a trend towards fibrosis improvement without worsening of NASH was observed, including 4% of patients in each of the EFX-treated groups who experienced a three- or two-stage improvement from F4 to F1 or F2 fibrosis. The trial demonstrated statistically significant results for NASH resolution, which we believe is the first such report, and statistically significant results on many other non-invasive markers of liver fibrosis. These results are consistent with previously reported EFX studies in patients with cirrhotic and pre-cirrhotic NASH, and continue to show EFX's potential to be an effective NASH therapeutic. Overall, though, no head-to-head comparative studies have been conducted, we believe these are the strongest data reported to date for any product in this difficult-to-treat population. The SYMMETRY study was designed to have two on-treatment biopsy reads for each patient: the 36-week analysis we are describing today and an end-of-treatment analysis at week 96. Given the trend in fibrosis improvement and the statistically significant results in NASH resolution and markers of liver injury at week 36, we believe another 60 weeks of treatment with EFX has the potential to yield higher rates of fibrosis improvement in cirrhotic patients at the completion of SYMMETRY. Additional context helps set the stage for today's data. First, patients with cirrhosis due to NASH face a poor prognosis. As seen here on slide 3, the overall five-year rate of survival without a liver transplant among F4 patients is about 50%. Not only is the survival prognosis poor, but as cirrhosis progresses to decompensation and liver failure, patients' quality of life is severely compromised. Put simply, cirrhosis is cancer-like in its potential morbidity and mortality impact on patients and in the economic burden it imposes on the healthcare system. Unfortunately, there are no approved therapies to treat cirrhosis due to NASH. Arresting progression to liver failure or reversing cirrhosis would therefore represent a major medical advance. With more than 3 million Americans estimated to have cirrhosis due to NASH by 2030, the unmet burden is high. Quite simply, any therapeutic that helps reverse fibrosis would be a game changer for a population with no other approved options. Second, meeting the pathology endpoints in patients with cirrhosis due to NASH has proved elusive. Slide 4 shows a landscape of some of the leading programs that have evaluated different mechanisms in Phase 2b or Phase 3 placebo-controlled trials in patients with cirrhosis due to NASH. Most of these programs have been discontinued. Development of semaglutide remains active, but the placebo-corrected rate was -18% for fibrosis improvement without worsening of NASH in a 48-week Phase 2b trial. Slide 5 shows a similar landscape for the NASH resolution endpoint. Here we see a 13% placebo corrected response rate for semaglutide, with no other mechanism higher than 6%. Importantly, each of the programs on these two landscape slides was studied for at least 48 weeks and as long as 96 weeks. The much higher proportion of collagen, accounting for 5%-35% of the area of a biopsy from cirrhotic liver, compared to up to 5% for pre-cirrhotic liver, represents a substantial challenge to address and helps account for the repeated program discontinuations in this indication. Against this backdrop, we believe the totality of today's SYMMETRY data stands out as perhaps the most promising publicly reported placebo-controlled data set to date in patients with cirrhosis due to NASH. 22% and 24% fibrosis improvement without worsening of NASH was observed for the EFX 28 and 50 milligram arms, respectively, compared to 14% for placebo. As mentioned earlier, 4% of EFX patients also experienced at least a two-stage reversal of fibrosis from F4 to F2 without worsening of NASH. There's also considerable evidence that EFX improved liver health. Notably, we observed that NASH was resolved in approximately 60% of EFX-treated patients, the first drug reported to show a significant effect on this endpoint in patients with cirrhosis due to NASH, compared to 26% for placebo. Likewise, non-invasive markers show that EFX reduced synthesis of new collagen and overall fibrosis to a similar extent seen in patients with moderate to advanced fibrosis, F2 and F3, as reported last week in Lancet Gastroenterology and Hepatology. Markers of liver injury were also significantly reduced, consistent with effects seen in pre-cirrhotic patients. Crucially, these improvements were sustained over 36 weeks, in contrast to the only other FGF21 analog, pegbelfermin, tested in a comparable patient population. Based on these observations, we are confident that EFX's anti-fibrotic effect is exerting clinical activity in cirrhosis and believe with longer treatment, EFX could potentially continue to reverse cirrhosis and improve overall liver health. The pre-specified 96-week biopsy analysis in SYMMETRY, scheduled for late 2024, will evaluate this. I'll now turn the presentation over to Kitty to walk through the study design and data in more detail. Thank you, Andrew, and good morning, everybody. I'd like to begin with a review of the design of the SYMMETRY study, which is shown in Slide 6. The SYMMETRY study is a Phase 2b randomized, double-blind, placebo-controlled, multicentered, dose-ranging trial. All patients had biopsy-proven compensated cirrhosis, fibrosis stage four, due to definitive NASH or cryptogenic cirrhosis, presumed secondary to NASH. Subjects with cryptogenic cirrhosis were limited to approximately 20% of the total study population. Importantly, the design of SYMMETRY allowed for an early efficacy evaluation at week 36, as well as an end of treatment evaluation at week 96. After the 36-week analysis, patients remain on their randomized treatment out to week 96, when they will receive an end of treatment biopsy. The study enrolled 182 patients, with approximately 60 in each treatment group, randomized to receive once weekly subcutaneous doses of either 28 or 50 milligrams of EFX or placebo. The primary endpoint was the proportion of subjects who achieved at least a 1-stage improvement in fibrosis without worsening of NASH at week 36. Secondary measures include NASH resolution, a combination of fibrosis improvement and NASH resolution, change from baseline in non-invasive markers of fibrosis, liver enzymes, glycemic control, lipoproteins, and body weight at 36 weeks, as well as safety and tolerability. Patient disposition is shown in Slide 7. 182 patients were randomized. 1 patient was randomized, but not dosed. 26 patients, or 14%, discontinued prior to week 36. 11 of the 26 discontinuations were described as being for other or administrative reasons. The remaining 15 patients discontinued due to adverse events, 2 in the placebo group, 5 in the 28 milligram group, and 8 in the 50 milligram group. Of the remaining 155 patients who completed week 36, 2 patients declined to be biopsied a second time. Thus, there were 153 patients in the liver biopsy analysis set used for the primary endpoint. Of these, 57, 46, and 50 were in the placebo, 28, and 50 milligram dose groups, respectively. This study enrolled patients with advanced liver disease, including patients with either cryptogenic cirrhosis or definitive NASH. The analysis set for NASH resolution endpoints excluded those with cryptogenic cirrhosis who didn't meet definitive NASH at baseline. That is a NAFLD activity score of greater than equal to 3, with a score of at least 1 in each of the components of steatosis, ballooning, and inflammation. Consequently, the analysis set for NASH resolution is comprised of 126 patients, with 46, 38, and 42 patients, respectively, in the placebo, 28, and 50 milligram dose groups. Cryptogenic cirrhosis is sometimes referred to as burnt out NASH and is associated with advanced fibrosis and a higher level of risk in terms of liver decompensation or death. On Slide eight, we review the baseline demographics, which are consistent with what has been reported in fibrosis stage four NASH clinical studies and are representative of the compensated cirrhotic patient population. The majority of patients were female. In this advanced patient population, 17%-26% of the patients had cryptogenic cirrhosis across the three treatment groups. The non-invasive markers of fibrosis, ELF, PRO-C3, and liver stiffness levels are higher than we had seen in our HARMONY trial and consistent with more extensive cirrhosis. AST and ALT values range from 35-40, with ratios approaching a 1-to-1. Approximately 80% of the patients had type 2 diabetes, and they were being extensively treated, with approximately one-quarter of patients receiving GLP-1. Serum triglyceride levels were borderline high, but lower than seen in precirrhotic patients in HARMONY. The advanced stage of disease was evident in the medical history of SYMMETRY patients, with the majority taking more than 10 concomitant medications to manage their comorbidities of NASH. Before diving into the histology results, it's important to highlight that we used the same biopsy analysis process that was used in HARMONY, and this is reviewed on slide nine. Our consensus approach in SYMMETRY was to have all biopsies read by two well-trained pathologists. Each pathologist scored each individual biopsy sample independently. Our pathologists were blinded to subject and treatment assignment. Biopsies were shuffled to ensure the pathologists were also blind to the visit sequence. Our protocol specified that if consensus couldn't be reached, a third trained pathologist would adjudicate between the two scores. All biopsy analyses were resolved by consensus, so adjudication was not required. On slide 10, we report the results of the primary endpoint of fibrosis improvement of 1 or more stages without worsening of NASH, which was observed in 24% for the 50-milligram dose group and 22% for the 28-milligram dose group, compared to 14% placebo response. These translate to treatment effect sizes of 8% and 10% in the 28- and 50-milligram doses, respectively. The table on the right highlights patients in each of the EFX-treated groups who experienced a greater than or equal to 2-stage improvement in fibrosis, improving from F4 to either F1 or F2. Despite the short treatment duration, we believe these response rates are numerically higher among those reported to date in placebo-controlled clinical studies in patients with compensated cirrhosis. We believe the trend here may lead to a higher treatment response with longer treatment out to week 96. Slide 11 reports the results for the percentage of patients who achieve NASH resolution. The rates of NASH resolution in both EFX treatment groups were statistically significant, with 60% or more NASH resolution. These response rates are more than double the 26% placebo response. We believe that re-reducing steatohepatitis, as indicated by NASH resolution, should ultimately, in time, lead to reversal of fibrosis and slow or arrest progression to liver failure. Using the intent-to-treat or ITT analysis set, which treats any missing data as failure, both EFX groups maintained statistical significance, with 47% of the 50 mg and 51% of the 28 mg group showing NASH resolution, compared to 24% for placebo. Slide 12 shows the percentage of patients in each group who achieved both fibrosis improvement of at least 1 stage and NASH resolution at the same time. 14% and 21% of the 50 mg and 28 mg EFX groups achieved both endpoints, compared to a 9% placebo control. On slide 13, current and discontinued programs reporting fibrosis improvement without worsening of NASH in patients with compensated cirrhosis have been arranged from left to right by study treatment duration. Information relevant to interpreting each dataset is provided above the corresponding histograms. Head-to-head trials comparing these various investigational drugs have not been conducted, so the differences in these trial designs and other factors make cross-trial comparisons challenging. Nonetheless, the effect sizes, meaning the difference between treatment and placebo for both doses of EFX, are among the highest reported to date. Slide 14 places the NASH resolution rates in the same landscape. As you can see here, and although cross-trial comparisons have inherent limitations, EFX is the only compound to demonstrate statistically significant improvement in NASH resolution in this patient population.... Non-invasive markers used to diagnose and monitor fibrosis and cirrhosis indicated that both doses of EFX decreased synthesis of new collagen and reduced inhibition of remodeling of fibrosis in a statistically significant manner. Slide 15 depicts change from baseline for the Enhanced Liver Fibrosis panel. The change from baseline is shown overall in the left-hand most histogram, with significant reductions in the EFX group relative to placebo after 36 weeks. The corresponding changes for each component of the panel are shown in the next three histograms. Moving left to right, these are P3NP, a marker of collagen synthesis associated with liver fibrosis, TIMP-1, a marker of inhibition of collagen remodeling, and hyaluronic acid, a major component of the basement membrane to which liver cells attach. EFX treatment groups showed statistically significant reductions in mean levels of P3NP and TIMP-1 at both doses, while the change in hyaluronic acid was not statistically significant. The extent of reductions in P3NP and TIMP-1 is comparable to what we observed in the 24-week HARMONY study in F2, F3 patients, as is the limited impact on hyaluronic acid. Moving on to slide 16, which depicts mean change from baseline for three more non-invasive fibrosis markers. The first histogram shows PRO-C3, another marker of collagen synthesis in the liver. The second plot shows liver stiffness measured by FibroScan, and the third histogram shows FAST, a score which combines liver stiffness and the liver injury marker AST, and is widely used to assess risk of NASH progression. Both doses of EFX showed statistically significant reductions in PRO-C3 relative to placebo, consistent with the reduction in P3NP. Moving to the middle plot, EFX reductions in liver stiffness were statistically significant relative to baseline. However, the reductions were not significantly different from placebo, which declined to a similar extent. This appears to be anomalous with, by reference to prior studies with EFX in precirrhotic and cirrhotic patients. In the rightmost plot, EFX shows statistically significant reductions in mean FAST score relative to placebo. Again, the extent of reduction from baseline in these markers is similar to what was observed in the HARMONY study. Moving on to slide 17, which depicts mean change from baseline for two markers of liver injury, ALT and AST. Baseline levels of these enzymes are lower in cirrhotic than precirrhotic patients because of the loss of normally functioning hepatocytes. Nevertheless, 50 mg of EFX significantly reduced both levels of enzymes relative to placebo, reaching a maximal effect between 12 and 16 weeks, which was then maintained undiminished throughout 36 weeks of treatment. The magnitude of reduction in ALT and AST was smaller for the 28-mg EFX group, but still significant relative to placebo at most intervals after 8 weeks. Substantial and maintained reductions in markers of liver injury have been consistently observed following treatment with EFX for periods of 16-36 weeks in patients with both cirrhosis and precirrhotic NASH. One of the goals of treatment for patients with cirrhosis is to prevent progression of disease to portal hypertension or decompensation. To that end, platelet count significantly decreased from baseline by around 7% in both EFX dose groups, compared to a slight reduction for placebo. Consistent with this trajectory of preventing progression, other markers of disease progression, including bilirubin, INR, MELD, and Child-Pugh score, remained stable or showed slight improvements. Let's shift now to safety and tolerability. Slide eighteen summarizes patients who discontinued from the study. Starting at the top of the table here, there was 1 death in a placebo patient who had pneumonia. 21 serious adverse events were reported, which were balanced across treatment groups and reflect the complex comorbidities of this advanced NASH population. The only event reported in more than 1 subject was angina, which occurred in 1 patient on placebo and 1 patient on the EFX 50 mg group. None of the SAEs reported were determined to be drug related by the clinical investigators. A total of 12 patients were discontinued due to drug-related adverse events, or, at, or AEs. 1 in the placebo group, 3 in the 28 mg group, and 8 in the 50 mg group. The majority of these were due to grade 1, 2 diarrhea, with 5 patients discontinuation due to diarrhea in the 50 mg EFX group.... one each for the placebo and the 28 milligram dose group of EFX. In the other category, for the 28 milligram group, one patient discontinued due to retching and vomiting, and the other due to palpitations and feeling jittery, which are likely symptoms of a relative hypoglycemia, which may occur with a fast-acting insulin sensitizer like EFX, particularly during the first months of treatment. In the 50 milligram group, one patient discontinued due to soft feces and nausea. Another patient discontinued due to a suspected allergic reaction with flushing, vomiting, and fatigue that was coded as hypersensitivity. The third patient discontinued due to a grade two patch of a rash at the injection site. There were three non-drug-related adverse events that led to treatment discontinuation. In the placebo group, one patient, as I mentioned before, died due to pneumonia. For the EFX 28-milligram, one patient with a history of cardiac disease experienced cardiac failure and required replacement of their pre-existing cardiac pacemaker. Another patient discontinued due to drug hypersensitivity related to one of their concomitant medications, diltiazem. Slide 19 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 grade 1-2 events. The majority of injection site reactions were mild grade 1. As reported in previous studies, even though we see increased appetite was reported as an adverse event, mean body weight reductions were observed across the EFX dose groups. No clinically meaningful changes were observed for heart rate or diastolic blood pressure. However, at week 36, increases of 4-7 millimeters of mercury in size, diastole, sorry, in systolic blood pressure were observed in the EFX dose groups. Based on non-clinical observations on skeletal development, bone health has been monitored in all clinical studies with FGF21 analogs. It's important to note that fatty liver disease is associated with poorer bone health, in part because of post-menopausal women who constitute a large proportion of the patient population. Small reductions in bone mineral density were observed for the EFX dose groups in the lumbar spine of less than 1% and in the femoral neck region in the range of 2%-3%. I'll now turn the presentation over to our Chief Scientific Officer, Tim Rolph. Thank you, Kitty, and good morning, everyone. By way of context to the effects of EFX on markers of glucose metabolism in patients with cirrhosis, shown on slide 20, almost 80% of the study population were being treated for type 2 diabetes, with a high proportion on medications to boost insulin levels. This slide depicts mean change in baseline and fasting levels of C-peptide, a marker of insulin secretion, insulin and glycosylated hemoglobin, or HbA1c. Treatment with both doses of EFX for 36 weeks showed statistically significant reductions in serum levels of C-peptide and insulin, consistent with EFX improving insulin sensitivity. EFX treatment was associated with reduced levels of hemoglobin A1c, but not significantly more than placebo. This may in part be attributable to this population of patients generally being well controlled, particularly with patients in the 50 mg EFX group, having a mean baseline HbA1c of 6.6%. It may also be attributable to a fourfold higher proportion of patients in the placebo group than the EFX groups, with poor glycemic control at baseline. That's a hemoglobin A1c of greater than 9%. To put the effects of EFX on serum lipids on slide 21 in context, pretreatment levels of triglycerides were at the high end of normal. Those of low-density cholesterol were generally close to goal of 100 mg/dL, reflecting the substantial proportion of patients taking statins, while those of high-density cholesterol were low, reflecting the high proportion of patients with diabetes. This slide depicts mean change in baseline. Treatment with 50 mg EFX showed statistically significant reductions in triglyceride and non-HDL cholesterol, and statistically significant increases in HDL cholesterol and numerically lower LDL cholesterol. The effects of treatment with 28 mg EFX followed a similar pattern to the higher dose, but the magnitude of improvement was slightly smaller. Moving on to slide 22, which shows mean change from baseline to serum adiponectin, a pharmacodynamic measure of agonism of FGF21's receptors, receptor rather, FGFR1c in adipose tissue. After 36 weeks of treatment with both doses of EFX, levels of adiponectin were approximately doubled, while placebo didn't change. EFX's beneficial effects on adipose tissue, enhancing insulin sensitivity, and reducing release of fatty acids, is key to establishing a healthy whole body metabolic environment in which hepatocytes are not overloaded with energy. This reduces hepatocyte stress and decreases the rate of loss of normally functioning hepatocytes. Slowing, or preferably preventing, further loss of normally functioning hepatocytes is essential to preservation of liver function and avoiding progression to failure in patients with compensated cirrhosis. Moving on to slide 23, which depicts change from baseline in body weight after 36 weeks treatment. By comparison with placebo, 28 milligram of EFX appeared to be weight neutral, while for the 50 milligram dose, body weight trended lower with a significant decrease from baseline. This pattern of response is consistent with that observed in three prior separate studies of EFX with pre-cirrhotic patients up to 16-24 weeks of treatment, including on top of stable GLP-1 receptor agonists. I will now hand over to Andrew to conclude the presentation. Thank you, Tim. In conclusion, we are encouraged by today's SYMMETRY data and believe it supports moving EFX forward into Phase 3 in patients with cirrhosis due to NASH. Although no head-to-head comparative studies have been conducted, we believe the totality of these data are the most encouraging report to date for this difficult to treat population. Despite the short treatment duration, we see a trend in fibrosis improvement, including 3-stage and 2-stage improvements for some patients. In addition, we have statistically significant results, both for NASH resolution and for many non-invasive markers of liver fibrosis. Based on these observations, we're confident that EFX has the potential to improve liver health and whole body metabolism in patients with cirrhosis. With $659 million in cash as of June 30, 2023, and runway into 2025 and 2026, we are well positioned to move ahead with our Phase 3 program. Specifically, we are pleased to have supportive data from our two placebo-controlled phase 2b studies to advance EFX into Phase 3 for both patients with NASH due to cirrhosis and patients with pre-cirrhotic NASH, fibrosis stages F2 and F3. Taken together, today's SYMMETRY study and last year's HARMONY study, in which over 300 patients have been treated with EFX, show that EFX has the potential to treat the core facets of NASH. EFX has been observed to reduce fibrosis, resolve NASH, improve non-invasive markers of liver injury and fibrosis, reduce liver fat, improve glycemic control and lipoprotein profile, and reduce body weight. These are the hallmarks of an investigational drug, well-matched to a complex disease affecting the whole body as well as the liver. The Phase 3 SYNCHRONY Histology and SYNCHRONY Real-World studies in patients with pre-cirrhotic NASH, stage F2 and 3, are well underway and remain on track to enroll the first patients by December 2023. We look forward to discussing today's SYMMETRY results with the FDA to help finalize plans for incorporating patients with cirrhosis due to NASH into our Phase 3 program. We are excited to continue developing therapies that have the potential to transform the lives of patients living with serious metabolic diseases. Thank you. To ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. The first question comes from Michael Yee with Jefferies. Your line is open. Morning. Yeah, two questions for you, Andrew. First, when you take a look at this study and step back, do you think it was a higher discontinuation rate and dropout rate that would have impacted this? What gives you confidence that a longer treatment duration would be helpful here? If I may ask a follow-up, there was disclosure on the slides around bone mineral density and a 5 or 4-7 millimeter increase in systolic blood pressure. Can you make a comment about that? That would be something I think that some people are capturing. Thank you. Yeah. So, I, Mike, I think the, as we mentioned during the call, overall, we're pleased with the totality of the data. The discontinuation rate was a little higher than we had expected, but at the same time represents the, to some degree, some of the overall, advanced disease that these patients have. In terms of you asked about blood pressure. Maybe Tim, if you want to make a comment about that, that'd be helpful. Yeah. The increase in systolic blood pressure appears to be associated with the reduced capacity of the liver in these patients to maintain blood glucose. So when they are exposed to a rapidly acting insulin sensitizer, their blood glucose levels vary quite markedly. And that's leading to activation of the regulatory hormones, glucagon, adrenaline, both of which are known to increase systolic blood pressure. We would expect, going forward into Phase 3, that we'll be using, adapting the doses of the antidiabetic medications to allow glucose to be better controlled in these patients. I guess, Andrew, to clarify, I was asking, what gives you confidence that longer treatment duration would boost the results in this study? Thanks, Mike. There were a number, I can get through all of them. So I think when one looks about at the mechanism of action, I think that it's really driven by the additional collagen that these patients have. It's just so much more than what we've seen in the pre-cirrhotic population. And when we look at the response rates, especially the deep response rates in the patients with two and three-stage improvements in fibrosis, it gives us the confidence that the mechanism is very active, and it just takes more time to reduce to get the collagen down from these higher percentages at baseline. Thank you. Please stand by for the next question. The next question comes from Eric Joseph with JP Morgan. Your line is open. Hi, good morning. Thanks for taking the questions. I too am just a little bit curious about sort of what gives you confidence in moving forward with a cirrhotic NASH Phase 3 program, based on the data here today, as opposed to perhaps getting a little bit more from the end of treatment assessment at 96 weeks. And then, this potential for cryptogenic NASH, I think, is a new variable in thinking about the conduct of an F4 study. I guess, what sort of, to the extent there are, are there any measures that could be taken in a Phase 3 program to sort of reduce their participation and perhaps get a you know, a clearer signal? Thank you. So Eric, thanks for raising that. So I think recall that the Phase 3 program, per the update guidance, is an outcomes-driven measure. So I think when one thinks about one stage improvement of fibrosis, that's not necessarily directly correlative with outcomes-based endpoints. And so I think for us on that, it's we think that we've seen improvements in liver health overall, and it's as well as improvements in NASH resolution that will also contribute to improvements in outcomes overall. In terms of cryptogenic cirrhosis, I think these patients represent as part of the cirrhotic spectrum, and they have a little more advanced NASH. And I think we've, in consultation with the FDA, have chosen to limit the patients to about 20% of the population. I think that's something we may consider to do, but of course, that's pending discussion with the agency, which we haven't had. Please stand by for the next question. The next question comes from Michael with Morgan Stanley. Your line is open. Hey, guys. Thanks for taking the question. Maybe just to follow up on the thinking in terms of the Phase 3 plan for F4 patients. Could you... I guess some of the scenarios around that, could you start that Phase 3 study near term, or, or would you want to see the results from the 96-week end of treatment SYMMETRY study, before you move forward there? Thanks. Mike, it's a good question. I think, you know, we think we have enough data to move forward in Phase 3, but it's important that we haven't consulted with the agency on this. We had an end-of-phase 2b meeting in March of this year, which we said that in pursuing the alternative pathway, where we use the F4 population outcomes-based approach as a confirmatory study, in principle, they were in agreement with that. But at the same time, we both sides agreed to say, "Let's come back and readdress this once we have SYMMETRY results." So, since we're announcing the results today, we haven't had a discussion with the agency. We are going to reach out to them and hope to talk to them in the near term. Got it. Makes sense. Thank you. Thanks. We have time for one more question. That question comes from Liisa Bayko with Evercore. Your line is open. Hi, just two questions from me. First of all, was it pre-specified to take out the cryptogenic NASH patients, and can you give us the data on an ITT basis? Oh, and one more. For FDA, for your phase three study, is a histology biopsy endpoint still on the table, or are you thinking more along the lines of an outcome study for the cirrhotics? Thanks. So, I think for the cirrhotics, you know, this is, as I mentioned with Mike's question, we're still discussing with the agency. I think the agency, at this point, doesn't view histology as an approvable endpoint. However, as you and I have discussed in the past, the EMA does view it that way. So I think how we reconcile that and call requires some discussion with the agency. So I think that that's a little bit of a TBD. In terms of the ITT, it's on the slide, Lisa, on the endpoint slides. We put that on the data. I don't have the slide right in front of me. I couldn't really tell you right off the top of my head. Maybe Kitty, if you have that, if you could just help Lisa. Yeah, Lisa, I'm just wanting to check whether it was for the primary endpoint, you wanted that data? Yeah. Sorry, maybe I missed it because there was different cuts going on. But just the- Don't worry. It's... So it was 13% for placebo, 18% for the 20 milligram, and 19% for the 50 milligram. Thanks. And then, just final question was on the cryptogenic cirrhotics. Was it pre-specified to exclude them from some of the analyses? Or, what was the plan there? Yes. Yeah, that was all pre-specified. Thank you. Go, Kitty. Thank you for participating in today's program. This does conclude the conference. You may now disconnect. Everyone, have a great day.