Expression of Smad7 is induced by TGF-β1, which, in turn, exerts its negative feedback mechanism by causing degradation of TβRI and Smads [25]; however, the overt expression of TGF-β1 and Smad3 and decreased Smad7 are mostly observed in renal [26], cardiac [27], and bleomycin (BMI) induced lung fibrosis [28]; this above evidence suggests that TGF-β1 acts by stimulating Smad3 to mediate fibrosis. This evidence concerns the gene SMAD3 and pulmonary fibrosis.