The maximum LDL-C reduction observed was 69% in the highest dose cohort. From a clinical standpoint, how do such reductions compare to outcomes achieved with current PCSK9 inhibitors, and what might this mean for long-term ASCVD risk in HeFH patients?

With PCSK9 protein reductions mirroring LDL-C declines, how reliable is PCSK9 as a surrogate marker for successful in vivo base editing, and could it serve as an early indicator of efficacy in future studies?

The trial revealed a strong dose-dependent relationship between total RNA administered and LDL-C reduction. How might this shape future dose selection strategies for Phase 2, especially in balancing efficacy and safety?

VERVE-102 was well-tolerated across all dose levels, with no serious adverse events and no ALT or platelet concerns. How significant is this in the broader context of gene editing safety, and what would regulators likely focus on as dosing escalates?

Given that VERVE-101 has shown editing durability approaching two years, what are your expectations for VERVE-102’s long-term efficacy, and how critical is follow-up data beyond 28 days in validating a 'one-and-done' approach?

VERVE-102 uses a proprietary GalNAc-LNP delivery system. What differentiates this delivery platform from other LNPs currently in clinical use, and how does its dual-receptor targeting potentially expand the patient population?

The trial enrolled individuals with either HeFH or premature CAD. From a practical and ethical standpoint, how should future studies stratify these populations, and how broadly might this therapy be applied outside of inherited hypercholesterolemia?

Verve anticipates an opt-in decision from Eli Lilly later this year. What are the key elements Lilly and regulators will evaluate when assessing whether VERVE-102 is ready for co-development, and how might this influence the competitive landscape for PCSK9 therapies?