These complexities notwithstanding, the potential for CaMKII inhibition to reduce arrhythmogenic outcomes has been demonstrated in animal models of a remarkably broad range of human diseases: from genetic channelopathies, such as catecholaminergic polymorphic tachycardia (CPVT), to etiologically complex pathologies such as heart failure, atrial fibrillation (AF), and ischemia/reperfusion injury (I/R). Here, CAMK2G is linked to atrial fibrillation.