In other studies, knockout of CaMKII has been shown to protect from pressure-overload LV dysfunction but not prevent LV hypertrophy.13 CaMKII knockout improved hepatic insulin signaling in obese mice, while enhanced CaMKII activation has been shown to induce hyperinsulinemia and glucose intolerance.14 Taken together, these data suggest a potential causal role for Camk2n1 in cardiometabolic disease. The gene discussed is CAMK2G; the disease is Glucose intolerance.