"Can you elaborate on how 4D-310 targets the genetic root of Fabry Disease, particularly its impact on cardiac manifestations, and how it compares to traditional enzyme replacement therapies?"

Considering the Kansas City Cardiomyopathy Questionnaire results, how does 4D-310 potentially enhance the quality of life for patients, especially those with severe cardiomyopathy symptoms?

Based on the interim data, how would you assess the safety and tolerability of 4D-310, especially in light of the resolved cases of atypical hemolytic uremic syndrome (aHUS)?

Given the promising results of 4D-310, how might this therapy change the current reliance on enzyme replacement therapy for Fabry Disease patients?

Can you discuss the significance of the cardiac biopsy findings, particularly the reduction in Gb3 substrate in cardiomyocytes, and its long-term implications for cardiac health in Fabry Disease?

Following these interim results, what are the anticipated next steps in the clinical development of 4D-310, and how might this influence its regulatory approval and availability to patients?

The trial showed significant improvements in echocardiography contractility assessments. How do these improvements in global longitudinal strain (GLS) translate into real-world benefits for patients with Fabry Disease

With the observed improvements in CPET peak VO2 assessments, what implications does this have for the overall physical health and lifestyle of Fabry Disease patients?