In LV, CaMKII-associated prohypertrophic and upregulation antihypertrophic components of cell cycle were downregulated, specifying mechanisms for reduced LV mass, whereas in EAT, diminished pro-obesogenic cell cycle pathways and classical complement associated with insulin resistance provide mechanistic insights into reduced adiposity and ameliorated insulin sensitivity of Camk2n1−/− rats. The gene discussed is CAMK2G; the disease is Insulin resistance.