After MI, the infarction area is dominated by inflammatory cells that release cytokines to induce CFs migration to the infarcted area and collagen synthesis and secretion to replace necrotic myocardial tissue.22, 23 Studies have shown that after MI, CFs undergo phenotypic transformation and acquire a myofibroblast phenotype, which express α‐SMA, for both fibroblasts and smooth muscle cells to maintain the function of the damaged myocardium.5 This study focused on understanding the role of TGFβ3 in post‐MI. The gene discussed is ACTA1; the disease is myocardial infarction.