We previously identified that, in addition to its canonical function as a potent caspase inhibitor in both the extrinsic and intrinsic apoptosis pathways, XIAP activates nuclear transcription factor (NFκB) in suppression of two mechanisms of cell death caused by anti-tumor immune effectors (antibodies and T cells), granzyme-mediated cell death and accumulation of reactive oxygen species. The gene discussed is XIAP; the disease is neoplasm.