Consistently, a number of CPVT2-related mutations that increase CASQ2 proteolytic degradation, preventing its Ca2+-buffering activity or impairing its ability to modulate RYR2 opening, were found to induce spontaneous Ca2+ release, DADs, and, ultimately, ventricular arrhythmia during β-adrenergic stimulation [6,7,8]. The gene discussed is RYR2; the disease is Ventricular arrhythmia.