Of specific interest, previous work has shown that in addition to other targets involved in AF pathogenesis, CaMKII phosphorylates Nav1.5 at Ser571 in both atrial and ventricular myocytes, directly augmenting INa,L and disrupting intracellular homeostasis of both Na+ and Ca2+ [8, 10, 38]. Here, CAMK2G is linked to atrial fibrillation.