Further evidence for an important role for NF-κB in mesenchymal identity in GBM was provided by the demonstration that RelB-mediated NF-κB signalling is a critical mediator of GBM cell migration and invasion stimulated by the SMAC (second mitochondrial activator of caspases) mimetic, BV6, a molecule that antagonizes the inhibitor of apoptosis proteins and also triggers cell elongation, migration and invasion in GBM [57]. The gene discussed is NFKB1; the disease is glioblastoma.