In myocardial infarction, miR-21 activates the TGF-β/SMAD pathway via suppression of TGF-β receptor III in the ischemic area, enhancing collagen production, upregulating α-SMA expression, and facilitating fibroblast differentiation into pathological myofibroblasts [84, 85]. The gene discussed is TGFB1; the disease is myocardial infarction.