The role of CaMKII-dependent induced increase in SR Ca2+ leak and ventricular arrhythmias was later confirmed by experiments by Gyorke’s group, which revealed that replacement of Ser2814 site of RyR2 by Ala -a non-phosphorylatable amino acid-prevents ouabain-induced Ca2+ leak and arrhythmias. The gene discussed is CAMK2G; the disease is Ventricular arrhythmia.