As such, the cIAPs occupy a unique position for regulating cell-cell communication via exogenous ligands (TNF, TRAIL), intracellular response against invading pathogens, and humoral immunity.3, 8 As IAP antagonist treatment results in the auto-ubiquitylation of cIAP1, and cIAP2 to various extents, with subsequent loss of the cIAPs via the ubiquitin-proteasome system,1, 9 IAP antagonists have the potential to interfere with multiple signaling and regulatory processes including immunomodulation, inflammation, and cancer cell survival. The gene discussed is TNF; the disease is cancer.