NF-κB in defense and disease ing lymphocyte activation (8). The chemotherapeutic agent etoposide also increases NF-κB levels and thereby induces A1/Bfl-1, which prevents cytochrome c release from mitochondria and activation of caspase-3 (9). By increasing the expression of antiapoptotic cellular proteins, NF-κB activation can thus reduce apoptosis in response to treatment with different chemotherapeutic agents. NF-κB also acts in the control of the cell cycle, which is a critical element in determining the degree of cellular apoptosis and proliferation. NF-κB activates the expression of cyclin D1, a positive regulator of G1-to-S-phase progression, by direct binding to multiple sites in its promoter (10). Inhibition of NF-κB activation can reduce cyclin D1 activity and subsequent phosphorylation of the retinoblastoma protein to result in delayed cell cycle progression. This impaired cell cycle progression can be rescued by ectopic expression of cyclin D1 (11). Thus, the suppression of apoptosis induced by NF-κB involves the regulation of multiple genes involved in different aspects of growth control.