Expression of IL-6 and IL-6R is enhanced after allo-HCT, DCs are the principal source of IL-6 dysregulation after allo-HCT, and blockade of IL-6 signaling by in vivo administration of anti-IL-6R mAb attenuates GVHD with significant expansion of Tregs and reduction of inflammatory Th1 and Th17 cells (87, 88). The gene discussed is IL6R; the disease is graft versus host disease.