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. Here, TGFB1 is linked to systemic sclerosis.