GFAP and neoplasm: When this was done in combination with CRISPR-cas9 induced Trp53 loss, mice developed gliomas in both hindbrain and cortex within 8 months suggesting that H3.3K27M mutation cooperates with Trp53 loss in gliomagenesis when they are present in embryonic neural precursor cells but not in adult neural precursors (given that no tumours were observed when these alleles were expressed under control of nestin and GFAP promoters) [77].