Zhang et al. (111) demonstrated that miR-26a-deficient mice exhibit increased myocardial fibrosis, whereas overexpression of miR-26a significantly inhibited myocardial fibrosis in vivo and Ang II-induced fibrogenesis in cardiac fibroblasts by directly targeting connective tissue growth factor and SMAD4 (111). This evidence concerns the gene SMAD4 and Myocardial fibrosis.