These include direct phosphorylation and indirect ROS-mediated oxidation, which subsequently trigger the formation of mitochondrial permeability transition pores and myocardial necrosis [8, 34], Studies have reported that sustained activation of CaMKII is considered to be a central intracellular trigger for various cardiac diseases [34, 35], there is evidence that sustained activation of CaMKII contributes to a large number of major cardiac diseases, such as heart failure, arrhythmias, and cardiomyopathic sudden death [36–38]. The gene discussed is CAMK2G; the disease is heart disorder.