TGF‐β1 induces the activation of fibroblasts to undergo a phenotypic transition to myofibroblasts, which are the effectors of the fibrotic state.7 A plenty of works have identified that TGF‐β1 is an important pro‐fibrotic factor that has been shown to induce EMT in pulmonary fibrosis.8 TGF‐β1‐induced EMT is mainly mediated by Smad‐dependent or Smad‐independent pathways.9 Thus, anti‐EMT pathway or the method of inhibiting of TGF‐β1 signalling could provide a novel potential target for the treatment of IPF. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.