Although we demonstrated that activation of Fas-deficient DCs was up-regulated by engagement of RANKL signaling, and that the single transfer of RANKL-stimulated DCs resulted in accelerated autoimmune arthritis in MRL/lpr mice [14], we speculated whether repeated transfers, but not single transfer, of RANKL-stimulated DCs modify peripheral tolerance and control autoimmunity in MRL/lpr mice. The gene discussed is TNFSF11; the disease is Autoimmunity.