TGF-β1 expression is particularly high in fibrotic areas of the lungs of patients with IPF, and activated TGF-β1 drives ECM components, such as COL1A1 (collagen 1), FN1 (fibronectin), and ACTA2 (α-SMA), to generate a profibrotic environment in the injured area [19,20,21,22,23]. This evidence concerns the gene FN1 and idiopathic pulmonary fibrosis.