Reconstitution of wild-type mice with bone marrow lacking XIAP/cIAP1/2 or cIAP1/2 in the myeloid compartment not only transferred a mild form of spontaneous arthritis but also promoted exaggerated innate immune cell-driven K/BxN serum-induced arthritic responses that were associated with enhanced IL-1β and TNF activity, respectively. The gene discussed is IL1B; the disease is arthritic joint disease.