The exposure of quiescent fibroblasts to a variety of profibrotic mediators, such as transforming growth factor-beta 1 (TGF-β1) and platelet-derived growth factor (PDGF), results in phenotypic differentiation into myofibroblasts, which causes excess deposition of extracellular matrix (ECM) during IPF progression (Yin et al. 2018; Xie et al. 2020). This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.