Related studies show that the incidence of CPVT is about 1/10,000 (Leenhardt et al., 2012), the mechanism of its occurrence primarily involves abnormal calcium homeostasis in cardiomyocytes, usually caused by delayed posterior depolarization induced by abnormal RyR2 channels or CASQ2 proteins under conditions of sympathetic excitation, which proceeds to the development of bidirectional or polymorphic ventricular tachycardia (Priori et al., 2013). The gene discussed is CASQ2; the disease is catecholaminergic polymorphic ventricular tachycardia.