Our study used a well-established murine myocardial infarction model of myocardial infarction and primary cardiac fibroblasts from neonatal mice to explore how MTA3 induces the transformation of fibroblast-to-myofibroblast transition (FMT) by regulating downstream E2F1 during cardiac fibrosis. The gene discussed is MTA3; the disease is myocardial infarction.