These findings suggested that IRW with an increase in ACE2 level and mitigation of the AT1R receptor via multiple signaling pathways including ACE2/AMPK/SIRT1/eNOS, ACE2/AMPK/GLUT4, and ATIR/ET-1/P38 MAPK in the mouse aorta might be a therapeutic agent in MetS. The gene discussed is ACE2; the disease is metabolic syndrome.