CAMK2G and metabolic syndrome: The autonomous activation of CaMKII by autophosphorylation explains these results to some extent, through the phosphorylation of RyR2 at Ser2814, leading to abnormal Ca2+ leakage from the sarcoplasmic reticulum [17]; however, additional understanding of the detrimental changes induced by MetS in the main components of the cardiac β-adrenergic signaling pathway, upstream from the well-known effectors PKA and CaMKII, is needed, and this study addressed this imperative.