MiR-92a upregulation in SSc fibroblasts and serum from SSc patients might be a consequence of TGF-β endogenous activation as increased miR-92a levels were evidenced in normal dermal fibroblasts stimulated with TGF-β and decreased expression levels were shown after inhibition of TGF-β with siRNA [60]. This evidence concerns the gene TGFB1 and systemic sclerosis.