It binds to the T4-binding sites on the TTR tetramer, reducing its dissociation into monomeric TTR, the substrate for ongoing amyloid formation.19 In a Phase 3 trial (ATTR-ACT), tafamidis treatment in patients with ATTRwt- and ATTRv-CM-related heart failure (HF) reduced all-cause mortality and cardiovascular hospitalization by around 30% compared with placebo, although the survival curves of patients treated with tafamidis or on placebo started to diverge only after 18 months. This evidence concerns the gene TTR and hydrops fetalis.