The proliferative potential, both in basal conditions and in response to FPR agonists, was higher in SSc fibroblasts than in normal fibroblasts, suggesting that SSc progressive fibrosis could be linked to an aberrant activation of FPR signaling induced by the upregulation of DII-DIII-uPAR88–92. The gene discussed is FPR1; the disease is systemic sclerosis.