In contrast, TRAF1’s ability to stabilize and recruit cIAP2 to immune signaling platforms is necessary for optimal NF-κB and MAPK activation and a mutation that disrupts the TRAF1/cIAP2 interaction reduces cIAP2 levels and lowers joint inflammation in a model of RA.22 The gene discussed is NFKB1; the disease is rheumatoid arthritis.