Our group found that local ACE2 overexpression in the myocardium ameliorated left ventricular remodeling and dysfunction via an enhanced conversion of Ang II to Ang-(1–7) in a rat model of DCM9, and chronic infusion of Ang-(1–7) improved cardiac remodeling and function by reducing myocardial fibrosis, myocardial hypertrophy and cardiomyocyte apoptosis in a rat model of DCM10. This evidence concerns the gene ANG and Myocardial fibrosis.