In IDH-mutant gliomas, IDH mutations promote histone methylation marks including H3K27me3 by epigenetic reprogramming (141) Meanwhile, in SHH-MB, EZH2-mediated H3K27me3 marks accumulate at NEUROD1 regulatory elements, suppressing NEUROD1 expression and maintaining tumor cells in an undifferentiated state (Figure 3b). Here, IDH1 is linked to glioma.