PFD blocks multiple fibrogenic pathways, most likely through inhibiting transforming growth factor-beta (TGF-β)-mediated fibroblast proliferation and differentiation, whereas nintedanib interferes with several IPF-related pathophysiological pathways and mainly blocks tyrosine kinase receptors to limit the secretion of fibroblast growth factor, platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) [6,8]. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.