In addition, the treatment of glioblastoma multiforme (GBM) cells with the chemotherapeutic agent temozolomide (TMZ) and normobaric hyperoxia shown that hyperoxia increased the cytotoxicity of the drug, reflected in a high cell death rate, which seemed to be caspase-dependent apoptosis as an increase in caspase 3 activity was observed, along with an increase in Bax/Bcl-2 ratio. This evidence concerns the gene BAX and glioblastoma.