While other studies have reported the dysregulation of some Gtl2-Dio3 miRNAs in cardiac disease models including myocardial infarction [21–24], these studies did not analyze expression of Gtl2-Dio3 miRNAs in models of chronic cardiotoxic insult (Ang II), dystrophic cardiomyopathies (mdx, DyW), or in the temporal progression of myocardial infarction (MI). This evidence concerns the gene AGT and heart disorder.