Metabolic gene mutations are increasingly recognized as key drivers of tumorigenesis across various cancer types, including gliomas. These mutations impair normal cellular metabolism and disrupt crucial regulatory processes that maintain epigenetic stability. In particular, genes such as Fumarate Hydratase (FH) and Succinate Dehydrogenase Complex Subunit C (SDHC) have been implicated in a subset of hereditary and sporadic cancers, where their loss leads to the accumulation of metabolic intermediates with oncogenic potential [1-2].