GBM therapies induce the activation of redox-sensitive transcription factors, including nuclear factor-κB (NF-κB), nuclear factor erythroid 2 p45-related factor 2 (Nrf-2), or HIF-1 that would up-regulate cell survival molecules belonging to the BCL-2 family of proteins and the Akt survival pathway. Here, HIF1A is linked to glioblastoma.