Importantly, studies have also demonstrated that ventricular arrhythmias and myofibrillar hypercontracture associated with ischemia–reperfusion injury are, at least in part, due to intracellular Ca2+ overload and increased calcium-calmodulin dependent protein kinase II (CaMKII) activity10,11. The gene discussed is CAMK2G; the disease is Ventricular arrhythmia.