Most DIPGs also contain a mutation in Histone H3 at lysine 27 (refs 57, 58), which might epigenetically trap cells in a progenitor state50 and prevent repression of Olig2 or Sox2; one study showed that a H3K27M DIPG patient tumour-derived cell line had increased Olig2 expression correlated with decreased H3K27 trimethylation at the OLIG2 locus, when compared with mouse forebrain-derived neurospheres59. Here, OLIG2 is linked to neoplasm.