In addition, the CPVT-linked A4860G mutation was found to depress RyR2 channel activity,39 whereas ventricular myocytes from A4860G knockin mice had reduced amplitude of systolic Ca2+ release with overloaded SR Ca2+ content, which randomly caused bursts of prolonged systolic Ca2+ release triggering early after-depolarizations.40 Here, RYR2 is linked to catecholaminergic polymorphic ventricular tachycardia.