A recent study has shown that the intact PTEN immortalized malignant glioma cell lines are susceptible to the combination of SAHA and the Bcl-2 inhibitors ABT-737, whereas PTEN mutations were not.[28] They also showed that inhibition of the PTEN/PI3K pathway by BKM-120 sensitized glioma cells for ABT-737.[29] The patient-derived GSC model we used in this study is known to harbor PTEN deletions due to loss of chromosome 10q [13, 14], and ensures that we tested the treatment efficacy in a setting of hyper-activation of the PIK3-pathway. Here, BCL2 is linked to malignant glioma.