Our results suggest that silencing of Mcl-1 does not substantially further enhance DNA-fragmentation in GBM cells that were exposed to ABT263/Crizotinib, suggesting that the effect of the combination treatment might be predominantly mediated by its effect on Mcl-1 and its associated intrinsic antagonist, Noxa (Fig. 3C–D). This evidence concerns the gene MCL1 and glioblastoma.