Alfazema N, et al. - Given that Camk2n1 expression is cis-regulated in left ventricle and fat and positively related to adiposity in the spontaneously hypertensive rat model of metabolic syndrome, researchers knocked out Camk2n1 in spontaneously hypertensive rats to examine its role in metabolic syndrome. Reduced cardiorenal CaMKII (Ca²⁺/calmodulin-dependent kinase II) activity, lower blood pressure, enhanced nitric oxide bioavailability, and attenuated left ventricle mass related to altered hypertrophic networks was found in Camk2n1^−/− rats vs spontaneously hypertensive rat. In human visceral fat, they found a correlation of CAMK2N1 expression with adiposity and genomic variants that enhance CAMK2N1 expression related to increased risk of coronary artery disease and type 2 diabetes mellitus. Overall, Camk2n1 was identified as a regulator of multiple networks that control metabolic syndrome traits.