The persistence of oxidative stress and inflammation causes an additional release of profibrotic cytokines such as TGF-β1, TNF-α and PDGF, which activate fibroblasts and cause their differentiation into myofibroblasts, with excessive collagen accumulation and interstitial remodeling, resulting in pulmonary fibrosis [6,17]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.