Upregulation of Ho-1 levels was shown to improve left ventricular ejection fraction and inhibit remodeling in diabetic rats with myocardial infarction, and in vivo and in vitro studies demonstrated that Ho-1 overexpression attenuated angiotensin II-mediated cardiac hypertrophy in these mice [74]. The gene discussed is HMOX1; the disease is myocardial infarction.