CAMK2G and heart disorder: Such binding moves CaMKII toward a Ca2+/CaM-dependent activation active state and a Ca2+/CaM-dependent activation through structural rearrangement of the inhibitory helix caused by Ca2+/CaM binding and the subsequent autophosphorylation of T287 [65], which will induce the excessive activity of CaMKII and dynamic imbalance of the calcium ions in the myocardial cell, eventually leading to heart disease and arrhythmias.