Recently, caspase-2-mediated suppression of the survivin gene, a general regulator of cell division and cytoprotection in tumor cells has been reported, and this process appears to associated with the proteolytic cleavage of the NF-κB activator, RIP1, suggesting that caspase-2 functions as an endogenous inhibitor of NFκB-dependent cell survival and contributes to suppression of tumorigenicity in vivo [179]. The gene discussed is NFKB1; the disease is neoplasm.