To explore the therapeutic implications of the proposed mechanism, we examined potential synergy of the KRAS inhibitor deltarasin39 with the IKKβ-specific inhibitor IMD-0354 or the HSP90/IKKα/IKKβ inhibitor 17-DMAG using TNF- or IL-1β-stimulated LLC murine and A549 human lung adenocarcinoma cells expressing pNGL (Fig. 9a, b). This evidence concerns the gene CHUK and lung adenocarcinoma.