The ability of Bosutinib to modify the TGF-β-mediated autocrine increased levels of TGF-β and of the TGF-β receptors may represent one mechanism for the antifibrotic effects that we observed in this model, however, since the levels of these genes remain upregulated compared to the levels measured in control animals, the available evidence indicates that the effects of Bosutinib on TGF-β-mediated skin and lung fibrosis are due to its suppression of the ability of Src/c-Abl kinases to mediate the downstream effects of TGF-β signaling. The gene discussed is TGFB1; the disease is pulmonary fibrosis.