Figure 4a shows that BV6 caused rapid downregulation of cIAP1, whereas XIAP levels only slightly decreased after longer exposure. To investigate the involvement of NF-κB in BV6/Drozitumab-induced cell death, we used glioblastoma cells that overexpress IκBα superrepressor (IκBα-SR).27 NF-κB inhibition protected against BV6/Drozitumab-induced loss of cell viability (Supplementary Figure 4A), demonstrating that NF-κB is required for BV6/Drozitumab-induced cell death. This evidence concerns the gene XIAP and glioblastoma.