We also know that nintedanib (a multiple tyrosine kinase inhibitor) downregulates ECM production and promotes autophagy in IPF fibroblasts while inhibiting TGFβ1 signaling, which confirms the role of autophagy in the regulation of IPF fibroblasts (synthetic phenotype) [38]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.