CPVT is most associated with autosomal dominant gain-of-function variants in the RYR2-encoded cardiac ryanodine receptor-2 (RyR2) and recessive variants in CASQ2-encoded calsequestrin-2 (CASQ2), both of which affect intracellular Ca2+ (calcium) handling properties upon adrenergic stimulation and have a potential to trigger delayed after-depolarizations (DADs) and arrhythmias [7,8]. The gene discussed is CASQ2; the disease is cardiac arrhythmia.