Please describe your clinical practice. How many patients with AATD do you see on a yearly basis? Could you talk to us about the standard of care?

How well do patients respond to treatment with alpha-1 antitrypsin augmentation, and how does it stand up to new and emerging treatment options?

How often do patients develop COPD, cirrhosis, neonatal jaundice or panniculitis? What’s the best treatment to prevent that from happening?

Could you talk to us about the unmet needs in this disease?

Could you please share your thoughts on the Phase 2 results, where:-Fibrosis regression was observed in 58% (7 of 12) of patients receiving 200 mg fazirsiran-Median reduction of 83% of Z-AAT accumulation in the liver-Reduction of 69% in histologic globule burden

 Please talk to us about the liver health biomarkers.The company reported at baseline, mean ALT concentrations above the upper limit of the normal range in all cohorts. After treatment, ALT concentrations decreased in all cohorts from week 16 through week 52. All 12 patients with ALT concentrations above the upper limit of the normal range at baseline had reductions to normal concentrations at week 52.Regression of fibrosis of at least 1 stage occurred in 7 of 12 patients receiving the 200-mg dose (cohorts 1 and 2), including 2 patients with cirrhosis, and in none of 3 patients with evaluable biopsies who received the 100-mg dose (cohort 1b). Two patients in cohort 2 had progression of fibrosis from baseline to week 48 (both from F2 to F3), although both had profound reductions in PAS-D globule burden (scores of 9 and 4 at baseline and 0 for both at week 48) and reduced ALT and γ-glutamyltransferase concentrations with treatment.

How likely would you be to switch patients to fazirsiran ?