Abnormal CaMKII activity has been observed in human and animal models of cardiovascular disease (e.g., heart failure, myocardial infarction, arrhythmia), and is thought to promote downstream dysfunction in excitation-contraction coupling, structural remodeling, cell death, and even transcriptional activation of inflammation factors (Maier and Bers, 2002; Swaminathan et al., 2012). The gene discussed is CAMK2G; the disease is Arrhythmia.