Recent studies have significantly advanced the understanding of the genomic and molecular landscape of meningiomas, which are the most common primary intracranial tumors. A pivotal study identified chromosomal alterations, particularly the loss of chromosome 1p and gain of 1q, as critical factors that could enhance the current CNS WHO grading system for meningiomas. Patients with WHO grade 1 tumors exhibiting 1p loss showed progression-free survival (PFS) rates comparable to those with WHO grade 2 tumors, suggesting that chromosomal analysis could refine prognostic assessments (ref: Landry doi.org/10.1001/jamaoncol.2025.0329/). Another significant finding categorized BAP1-altered meningiomas as a distinct and aggressive subtype, characterized by recurrent loss of chromosome 3p21 and dysregulation of Polycomb repressive complex target genes, indicating a need for tailored therapeutic strategies (ref: Sievers doi.org/10.1093/neuonc/). Furthermore, the presence of chromosomal polysomies was linked to a distinct methylation signature and a lower risk of recurrence, highlighting the complexity of meningioma biology (ref: Vormittag-Nocito doi.org/10.1016/j.modpat.2025.100775/). These findings collectively underscore the importance of genomic profiling in understanding meningioma behavior and guiding treatment decisions. In addition to chromosomal alterations, somatic mutations such as AKT1 have been implicated in clinical outcomes, particularly in relation to preoperative seizures (ref: Dedhia doi.org/10.1227/neu.0000000000003445/). The evaluation of CDKN2A copy number status has also been emphasized, as its deletions are associated with malignancy and poor prognosis, although the accuracy of current assessment methods remains a concern (ref: Zschernack doi.org/10.1007/s11060-025-05029-6/). Overall, the integration of genomic data into clinical practice is poised to enhance the precision of meningioma management, facilitating better patient stratification and targeted therapies.