Since both proteins are major players in (E-C) coupling, the functional derangements in intracellular Ca2+ handling resulting from the mutated RyR2 and CASQ2 may cause delayed afterdepolarizations (DADs) and triggered arrhythmias which constitute the electrophysiological mechanism underlying CPVT 1–3. This evidence concerns the gene CASQ2 and catecholaminergic polymorphic ventricular tachycardia.