SMAD3 and pulmonary fibrosis: However, the constitutive activation of STAT3 via the Y757F point mutation in pg130 in a mouse pulmonary fibrosis model not only promotes fibrosis in the absence of the TGF-β signaling molecule SMAD3, which is well-known to be crucial in the pathogenesis of lung fibrosis [188], but also results in desmoplasia formation and epithelial stiffness, which enhance tumorigenesis in PDAC mouse models [186].