The proinflammatory mediators implicated in the physiopathology of ILD and SSc-ILD are represented mainly by transforming growth factor beta (TGFβ), platelet-derived growth factor, endothelin-1 (ET-1) and vascular endothelial growth factor, which eventually lead to microvascular dysfunction due to increased vascular permeability and the activation of fibroblasts. This evidence concerns the gene TGFB1 and interstitial lung disease.