In the present study, we provided evidence that the combination of CPX and BTZ led to the degradation of the NF-κB inhibitor, IκBα, and significantly enhanced activation of NF-κB signaling compared with these effects via CPX or BTZ alone, and dramatically upregulated NF-κB target genes (such as IL-6 and IL-8) in GBM cells. This evidence concerns the gene NFKB1 and glioblastoma.