In contrast, in intact hearts from a homozygotic CPVT mouse model exhibiting compromised Nav1.5 function, flecainide, despite being a Nav1.5 blocker, mediated anti-arrhythmic effects likely via the inhibition of RyR2-mediated Ca2+ release [6,7,16,33]. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.