Here, we found that Fed inhibited IL-6- or TGF-β1-induced abnormal wound healing of epithelial cells and fibroblast-to-myofibroblast transition, reduced TGF-β1-induced myofibroblast activation and accumulation and, finally, alleviated bleomycin-induced mice pulmonary fibrosis and inflammation. The gene discussed is TGFB1; the disease is pulmonary fibrosis.