Incubation of ISO-challenged CPVT VMs with mitoTEMPO restored SR Ca2+ content and reduced spontaneous Ca2+ release (Fig. 7), which implies that oxidation of RyR2 secondary to genetically evoked gain of function of SR Ca2+ release plays a key role in Ca2+-dependent arrhythmia. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.