Fibrosis and apoptosis show several links in SSc, as increased serum levels of the soluble form of the proapoptotic protein Fas have been reported in SSc patients [5]; pathological fibroblasts show resistance to Fas apoptosis [6], and mice lacking Fas or Fas ligand (FasL) genes [7], or treated with anti-FasL antibodies [8], show diminished apoptosis and a concomitant decrease in fibrosis and collagen accumulation. This evidence concerns the gene FASLG and systemic sclerosis.