The original work using GM-CSF/IL-4 to propagate a DC population from bone marrow progenitors, two decades ago, clearly established that BM-DC, as functionally immature cells in their ability to stimulate significant T-cell proliferation, induced donor-specific hyporesponsiveness to alloantigens in transplantation models (123–127) and also were able to prevent the onset of autoimmune disease, T1D in particular (128–131). The gene discussed is CSF2; the disease is autoimmune disease.