This autonomous activity of CaMKII can also be mediated by other post-translational modifications such as oxidation, nitrosylation, and glycosylation [105] The altered hyperactivate regulation of CaMKII is increased in myocardial disease, contributing to apoptosis, arrhythmias [113], defective ECC, and ETC (excitation–transcription coupling) [53,114,115], favouring pathological hypertrophy [96] and contractile dysfunction specifically during heart failure (HF) [54,96,114,115]. The gene discussed is CAMK2G; the disease is myocardial disorder.