To test the prediction that inhibition of both MCL-1 and BCL-XL is required to promote glioma apoptosis, we utilized a library of molecularly diverse patient-derived gliomaspheres (n = 26), which retain the genetic features and tumour initiating potential of GBM patient tumours (Supplementary Data Fig. 1B)18. Here, BCL2L1 is linked to glioma.