Constitutively active STAT3 confers resistance to apoptosis by enhancing transcription of anti-apoptotic regulators including Bcl-2, Bcl-XL and Mcl-1 (Fig. 1B) [62], whereas inhibition of STAT3 selectively induced apoptosis in WP1066-treated GBM cells by downregulating expression of anti-apoptotic genes and restoring BAX activity [65]. Here, BCL2L1 is linked to glioblastoma.