Other studies reveal that overexpression of iNOS in cardiac myocytes resulted in increased myocardial peroxynitrite, myocardial fibrosis, and ventricular hypertrophy, but ablation of iNOS shows less severe myocardial infarction-induced left ventricular remodeling compared to wild-type mice [38, 39]. The gene discussed is NOS2; the disease is cardiac hypertrophy.