It is well accepted that alterations in intracellular Ca2+ handling, due to functional abnormalities of mutant RyR2 channels, have a role in triggering arrhythmias in CPVT hearts, and Ca2+-dependent delayed after-depolarizations (DAD) have consistently and causally been linked to triggering arrhythmias in various murine models, harboring different CPVT-linked mutations [7,31,32,33,34]. Here, RYR2 is linked to cardiac arrhythmia.