Many profibrotic cytokines, chemokines, and pro-inflammatory mediators such TGF-B, platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) have been implicated to have a role in the pathogenesis of SSc-ILD through the activation of lung fibroblasts [8-11]. This evidence concerns the gene TGFB1 and systemic sclerosis.