Excess ROS release activates calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated hyperphosphorylation of ryanodine receptor 2 (RyR2), which could result in increased sarcoplasmic reticulum (SR) Ca2+ leak, delayed afterdepolarizations (DADs), and subsequent AF occurrence [12, 13]. The gene discussed is RYR2; the disease is atrial fibrillation.