SMAD3 and pulmonary fibrosis: Because EMT induced by TGF-β1 is a key issue in the pathogenesis of tissue or organ fibrosis [11]–[13] and inhibition of TGF-ß1 or Smad 2/3 could reverse EMT in hepatic fibrogenesis [58], drugs or targets of TGF-β/Smad3 pathway might be a suitable approach for pulmonary fibrosis therapy.