To understand which molecular mechanisms might cause differential TRAIL/TL32711 responsiveness, we analysed the expression amounts of key signal transduction regulators of the extrinsic and intrinsic apoptosis pathways (TRAIL receptors 1 and 2, FADD, procaspase-8, cFLIP, Bid, Bcl-2, Bcl-xL, Mcl-1, Bax, Bak, cytochrome-c, Smac, Apaf-1, procaspase-9, XIAP, and procaspase-3) that have already been reported for these GBM cell lines9. This evidence concerns the gene TNFRSF10A and glioblastoma.