Further molecular refinement revealed the enrichment of missense mutations and deletions in histone-lysine N-methyltransferase 2A (KMT2A) or MLL and histone deacetylase (HDAC) family genes within Cluster M2, underscoring the role of chromatin remodeling in GBM pathogenesis.22 Additionally, Cluster 3 has a greater frequency of p53 mutations, along with IDH1 wild-type and 1p/19q deletions, further distinguishing high-risk subgroups with aggressive tumor behavior.23 This evidence concerns the gene HDAC9 and glioblastoma.