To strengthen further the validity of targeting NF-κB and gap junction in GB therapy, we hypothesized that a) GB cells should express higher levels of components of the NF-κB signalling machinery and gap junction-forming connexin proteins than healthy brain and b) there should be a correlation between NF-κB molecules and connexin on the one hand and tumour aggressiveness and reduced survival on the other. This evidence concerns the gene NFKB1 and neoplasm.