Recent studies have significantly advanced our understanding of the molecular and genetic landscape of meningiomas, particularly in relation to their aggressiveness and treatment outcomes. One pivotal study identified increased mRNA expression of CDKN2A as a transcriptomic marker of clinically aggressive meningiomas, revealing that homozygous deletions of CDKN2A/B, although present in only 7.1% of cases, were linked to significantly poorer outcomes (ref: Wang doi.org/10.1007/s00401-023-02571-3/). Additionally, the study by Huo highlighted nine malignant progression-related genes that serve as prognostic signatures, emphasizing the need for further exploration of molecular characteristics in malignant meningiomas (ref: Huo doi.org/10.1038/s41598-023-28996-0/). Furthermore, Furtak's research uncovered a correlation between the NF2 mutation and tumor location, with most parasagittal tumors exhibiting this mutation, while sphenoid ridge tumors did not, suggesting distinct biological behaviors based on tumor location (ref: Furtak doi.org/10.1007/s00701-023-05567-w/). Barresi's findings on atypical meningiomas proposed a classification into four molecular groups, with hypermetabolic and proliferative groups showing the worst prognoses, thus providing a framework for future therapeutic strategies (ref: Barresi doi.org/10.1007/s00428-023-03537-2/). Collectively, these studies underscore the importance of molecular profiling in predicting outcomes and tailoring treatment for meningioma patients.