Nintedanib reduced pulmonary fibrosis by inhibiting growth-factor-induced proliferation (151) and motility (150) of lung fibroblasts, TGF-β-induced transformation of fibroblasts to myofibroblasts, EMT with increased E-cadherin levels (152), and ECM collagen secretion and ECM deposition (40), and reducing fibrotic gene expression (including collagen 1a1 and fibronectin) (153). The gene discussed is TGFB1; the disease is pulmonary fibrosis.