However, recent findings such as IκBα-independent NF-κB activation through NFKBIA (the gene coding for IκBα) deletion in most glioblastomas [16] or resistance to proteasome inhibitors in in vivo models [17] highlight the potential interest of inhibitors that act downstream of the IkB phosphorylation/degradation process. The gene discussed is NFKBIA; the disease is glioblastoma.