A previous study demonstrated that stress-response kinase JNK in the atria was involved in arrhythmic remodeling by activating calcium/calmodulin-dependent protein kinase (CaMK) II and, in turn, up-regulating diastolic sarcoplasmic reticulum calcium leak, leading to aberrant intracellular waves and enhanced AF propensity [41]. This evidence concerns the gene CAMK2G and atrial fibrillation.