The development of tissue fibrosis in patients with SSc is a complex process involving endothelial cell dysfunction and inflammatory cells (macrophage) activation that lead to the upregulation of pro-fibrotic cytokines such as TGF-β.[1] Dermal (or lung) fibroblasts and myofibroblasts accumulate in the tissue, leading to increased ECM deposition and fibrosis. This evidence concerns the gene TGFB1 and systemic sclerosis.