Objective：This study aims to explore the effect of c-FLIP（L）in pulmonary fibrosis and its pathological mechanism. Methods：Based on bleomycin（BLM）induced idiopathic pulmonary fibrosis in mice，the expressions of c-FLIP and E-cadherin were analyzed by IHC staining. Further investigations in A549 cells overexpressing c-FLIP（L），the expression levels of E-cadherin，N-cadherin and Vimentin mRNA were examined by qRT-PCR，and Smad activation induced by transforming growth factor （TGF）-β1 was detected by luciferase reporter assay and Western blot. Results：The increased c-FLIP expression was observed and associated with a decrease of E-cadherin expression. C-FLIP（L） overexpression resulted in the changes on E-cadherin，N-cadherin and Vimentin expressions in A549 cells. Furthemore，overexpression of c-FLIP（L） enhanced TGF-β-induced Smad activation，and knocking down c-FLIP（L） blocked the TGF-β1-induced EMT progress. Conclusion：C-FLIP（L） may be a promoting factor in the development of fibrosis via regulating EMT progress.