CPVT has been associated with mutations in various Ca2+ handling proteins, which lead to abnormalities in Ca2+ homeostasis; most notably, these mutations are found in the cardiac ryanodine receptor-Ca2+ release channel (RyR2) [25, 35] and the sarcoplasmic reticulum (SR) Ca2+-binding protein calsequestrin 2 (CASQ2) [13, 19]. This evidence concerns the gene CASQ2 and catecholaminergic polymorphic ventricular tachycardia.