In SSc an increased production of pro-inflammatory and pro- fibrotic cytokines is observed, particularly TGFβ, IL-1 and IL-6, which are also linked to Th17 differentiation; this leads to hypothesize that SSc pathogenesis may be related to a polarization of the immune response toward the Th17 pathway 12, and to suggest IL-17 as a possible therapeutic target. This evidence concerns the gene TGFB1 and systemic sclerosis.