The arrhythmogenic activity similar topost-depolarization and delayed post-depolarization induced by cytosolic andmitochondrial Ca2+ overload and oxidative stress mediated by L-type Cavin ventricular cardiomyocytes by a mechanism dependent on calmodulin II (CaMKII) canbe suppressedby the use of resveratrol37,just as atrial fibrillation induced bycoronary artery ligation in rabbits can bereduced by regulating ion channels via phosphoinositide 3-kinase (PI3K)/AKT/eNOSsignaling pathway39. Here, AKT1 is linked to atrial fibrillation.