CDNK2A deletion is common in human high-grade glioma, and we observed that additional CDKN2A loss in the mouse model was required for the induction of GBM by the combination of kRas and Akt3. However, the combination of kRas and Akt1 signals was sufficient to induce GBM in Ntv-a mice [29, 30]. This evidence concerns the gene AKT1 and glioblastoma.