While the silencing miR-223 inhibits TGF- β1-induced expression of collagen I, collagen III, and a-SMA proteins, and the over-expression of miR-223 and downregulation of its target recombinant Ras GTPase activating protein 1 (RASA1) promote the phosphorylation of MEK1/2, ERK1/2, and AKT in cardiac fibroblasts, indicating that miR-223 can promote proliferation, migration, and differentiation of cardiac fibroblasts by down-regulating RASA1 expression and activating the renin-angiotensin system (RAS) signaling pathway, thereby aggravating cardiac fibrosis after MI (Liu et al., 2018a). The gene discussed is AKT1; the disease is myocardial infarction.