Cardiac fibrosis is an important pathological process contributing to the pathogenesis of cardiac remodelling after MI, which is a transition from an early inflammatory phase to fibrotic granulation and maturation stage of cardiac remodelling.6 As a matter of fact, myocardial fibrosis is the end‐points of cell differentiation, activation and proliferation of cardiac fibroblasts.33, 34 Our study firstly explains the molecular mechanism by how TGF‐β induces cell differentiation of cardiac fibroblasts in myocardial remodelling through Prrx2 up‐regulation. The gene discussed is TGFB1; the disease is myocardial infarction.