Moreover, over-expression of constitutively activated IKBα S32A/S36A mutant (protein inhibitor of NF-κB) or siRNA-mediated silencing of Smad2/3 expression also generated effect similar to IKKβ or TGF-β receptor inhibitor in GBM cell lines, respectively (Supplementary Figure S5A, S5B). The gene discussed is NFKB1; the disease is glioblastoma.