Meanwhile, myofibroblasts release cytokines TGF-β, angiotensin II (Ang-II) and platelet-derived growth factor (PDGF) in an autocrine manner, which further stimulate cardiac fibroblasts to transform into myofibroblasts that express α-SMA in large amounts to further promote myocardial fibrosis to prevent cardiac rupture [62–64]. The gene discussed is ACTA1; the disease is Myocardial fibrosis.