Hyperglycemia-induced activation of CaMKII occurs via O-GlcNAc modification and induces spontaneous Ca2+ leak in isolated rat cardiomyocytes, premature ventricular contractions in ex vivo rat hearts, and increased arrhythmia susceptibility in diabetic rats during a caffeine stress test (Erickson et al., 2013). The gene discussed is CAMK2G; the disease is Hyperglycemia.