These mutations alone do not initiate tumor formation but act alongside additional genetic changes.101 The H3K27M mutation inhibits the polycomb repressive complex 2 chromatin-modifying complex, influencing the transcriptional programs associated with pediatric GBM.102 Enhancer of zeste homolog 2 (EZH2) overexpression further drives oncogenic pathways, including c-Myc activation, which is correlated with poor prognosis. The gene discussed is MYC; the disease is glioblastoma.