It could be hypothesized that GILZ inhibition of NF-κB and AP-1 transcriptional activity15,21 may prevent the development of tumor growth via inhibition of proinflammatory cytokines (Fig. 4), despite the fact that DEX-induced NF-κB inhibition may result in unresponsiveness of tumor cells to chemotherapy2. The gene discussed is NFKB1; the disease is neoplasm.