Additionally, genetic alterations like IDH1/IDH2 mutations (68, 69) and epigenetic changes such as mutations in histone H3 genes (70), along with aberrant transcriptional activity (71, 72) and disrupted metabolism (16) intertwined with signaling pathways (73, 74), collaboratively impact the cellular origin, oncogenic state, tumor aggressiveness, and response to therapy (33, 75). This evidence concerns the gene IDH2 and neoplasm.