It is known that the atrial activity of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is higher during sepsis and causes hyperphosphorylation of cardiac ryanodine receptor 2 (RYR2) channels preventing neuronal excitotoxicity, smooth muscle relaxation, vasodilation, and immunomodulation [46]. Here, CAMK2G is linked to Sepsis.