TNFR-stimulated noncanonical NF-κB activation involves ubiquitin-dependent degradation of TRAF3 or TRAF2.105 Importantly, pharmacological inhibition of cIAPs or genetic ablation of TRAF2 or TRAF3 causes constitutive activation of noncanonical NF-κB.117 Consistently, small molecule inhibitors of cIAPs (or smac mimetics) promote T cell activation and effector function and augment antitumor immunity.118–120 These studies implicate cIAP inhibitors as new therapeutic agents in combinatorial cancer immunotherapy. The gene discussed is TRAF2; the disease is cancer.