Unlike gliomas, which have been the focus of extensive immunophenotypic and transcriptomic subclassification, molecular classification of meningiomas has historically lagged behind [52,53,54], Emerging genomic subgroups, including NF2-inactivated tumors, 1p/22q co-deleted lesions, and non-NF2 mutant subsets such as those harboring AKT1, SMO, PIK3CA, or KLF4 mutations, are reshaping treatment paradigms by integrating biological behavior into clinical decision-making [47,48,49,50]. This evidence concerns the gene NF2 and meningioma.