If bone marrow failure and/or autoimmunity-mediated EPC destruction, but not secretion of mobilizing factors by the skin, represented the major bottleneck for a defect repair process in SSc, an aggressive angiogenic response with mouse progenitor cells and, therefore, increased mouse PECAM-1, in the SSc grafts would be expected. The gene discussed is PECAM1; the disease is Autoimmunity.