CAMK2G and metabolic syndrome: Together with our demonstration that visceral fat CAMK2N1 expression increased in obese subjects and correlated with adiposity and our analysis of cis-acting variants that regulate human CAMK2N1 and MetS traits, we conclude that Camk2n1 regulates multiple cardiovascular and metabolic processes, both dependently and independently of CaMKII, suggesting that endogenous Camk2n1/CAMK2N1 may not function exclusively as an inhibitor of CaMKII and requires a reappraisal of existing studies that have used nonspecific CaMKII inhibitors proposed to mimic Camk2n1 function.