Systemic sclerosis (SSc), rheumatoid arthritis (RA), polymyositis/dermatomyositis (PM/DM), and Sjögren’s syndrome (SS) may promote inflammatory responses in lung inflammation through TGF-β, TGF-β-mediated pulmonary fibrosis, by mediating myofibroblast activation, proliferation, and ECM protein deposition [14,15,16,17]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.