Here, we found that (a) human MI samples had the higher levels of TGFβ3 than normal samples; (b) TGFβ3 inhibited the migration, proliferation of human CFs, and certain concentrations of TGFβ3 attenuated collagen synthesis and the related protein expressions in human CFs; (c) TGFβ3 promoted the phenotype shift of human CFs and collagen cross‐linking; (d) TGFβ3 affected myocardial fibrosis via TGFβ/smad signalling, in which smad7 might be involved. The gene discussed is SMAD7; the disease is Myocardial fibrosis.