While this is a well-accepted mechanism causally linking, at the single-cell level, the gain of function of CPVT mutant RyR2 to transient diastolic SR Ca2+ leak and membrane depolarization caused by DADs, how the altered cellular function causes CPVT at the whole-heart and in vivo level is less well understood. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.