Given the suppression of Mcl-1 by THZ1, it was tempting to speculate whether THZ1 and BH3-mimetics would induce synergistic reduction in cellular viability in GBM model system given the long list of evidence that Mcl-1 is the primary mediator of resistance for BH3-mimetics that target either Bcl-2 or Bcl-xL. This evidence concerns the gene MCL1 and glioblastoma.