Recent studies have provided significant insights into the molecular and genetic landscape of meningiomas, particularly focusing on the mutational profiles and their implications for tumor behavior. One study utilized single-cell DNA sequencing to elucidate the order of mutational acquisition in meningiomas with TRAF7/AKT1 and TRAF7/KLF4 mutations, revealing that mutations with higher variant allele frequencies (VAFs) are typically acquired earlier than those with lower VAFs (ref: Dogan doi.org/10.1007/s00401-022-02485-6/). Another investigation identified two predominant molecular subtypes of spinal meningiomas, highlighting a strong association between thoracic NF2-mutant tumors and female sex, while cervical AKT1-mutant tumors were found to originate ventral to the spinal cord (ref: Hua doi.org/10.1007/s00401-022-02474-9/). These findings underscore the importance of genetic profiling in understanding the clinical behavior of meningiomas and tailoring treatment strategies accordingly. Additionally, the role of epigenetic changes in meningioma progression has been explored, with one study employing methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) to investigate genomic and epigenomic instability in matched primary and recurrent meningiomas (ref: San-Miguel doi.org/10.3390/cancers14164008/). The study found that alterations in cell-death programs contribute significantly to tumor progression. Furthermore, transcriptomic analyses have identified dysregulated gene modules in grade 2 meningiomas, correlating with EZH2 expression and suggesting that these molecular signatures could serve as predictive markers for tumor behavior and patient outcomes (ref: Pereira doi.org/10.3171/2022.7.JNS22953/). Overall, these studies highlight the intricate genetic and molecular mechanisms underlying meningioma pathogenesis and their potential implications for clinical management.