These include long QT syndrome 3 (LQT3) arising from a gain-of-function mutation in the cardiac sodium NaV1.5 channel gene SCN5A, Brugada Syndrome (BrS) arising from a loss-of-function mutation in the SCN5A gene, and catecholaminergic polymorphic ventricular tachycardia (CPVT) arising from a gain-of-function mutation in RyR2 gene or loss-of-function mutation in CASQ2 gene encoding cardiac calcium homeostasis proteins (23, 24). This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.