This activation manner still requires the initial binding of the Ca2+/CaM complex to the CaMKII regulatory domain to release the self-inhibitory structure, and the oxidized component is ROS produced by pathological stimuli or factors such as hyperglycemia, activation of the renin–angiotensin–aldosterone system (RAAS), MI, or heart failure (HF) (Erickson et al., 2008; Luo et al., 2013). Here, CAMK2G is linked to myocardial infarction.