TP53 and glioblastoma: Finally, proneural tumors show alterations in the PDGFR, IDH1, and TP53 as well as high expression of oligodendrocytic development genes, such as PDGFRA, NKX2-2, and OLIG2. Importantly, Bcl2L12 exhibited low-level amplification and expression in the proneural class harboring p53 pathway mutations, and higher amplification and expression in EGFR-driven classical and mesenchymal subtypes [36, 37], suggesting that tumors with already incapacitated p53 signaling circumvent the need for additional gain of the p53 inhibitor Bcl2L12, thus providing genetic evidence of a Bcl2L12-p53 axis in GBM.