In both cell cultures, namely, oxygen-glucose-deprivation (OGD)-treated CMs and H9c2 cells and an in vivo MI mouse model, miR-26a overexpression decreases collagen 1, CTGF, and ATM (Ataxia-telangiectasia mutated) expression levels, reducing cardiac fibrosis and apoptosis [134]. The gene discussed is CCN2; the disease is myocardial infarction.