Recent studies have significantly advanced the understanding of the molecular and genetic landscape of meningiomas, particularly through the identification of distinct molecular subgroups. Youngblood et al. explored the associations between these subgroups and tumor recurrence, revealing that integrated genomic and epigenomic analyses could inform clinical prognostication and treatment optimization (ref: Youngblood doi.org/10.1093/neuonc/). Williams et al. expanded on this by presenting a genomic survey of high-grade/progressive meningiomas, identifying three subclasses based on NF2 mutation status, which underscores the heterogeneity of aggressive meningiomas and the need for tailored therapeutic approaches (ref: Williams doi.org/10.1186/s40478-020-01040-2/). Furthermore, Schieffer et al. highlighted a rare subset of childhood and young adult meningiomas characterized by a YAP1-FAM118B fusion, indicating that genetic drivers beyond NF2 are crucial in understanding the pathogenesis of these tumors (ref: Schieffer doi.org/10.1097/PAS.0000000000001597/). Teranishi et al. improved diagnostic rates for mosaic neurofibromatosis type 2 (NF2) through targeted deep sequencing, emphasizing the importance of comprehensive genetic testing in atypical presentations of meningiomas (ref: Teranishi doi.org/10.1136/jmedgenet-2020-106973/). Chen et al. introduced a novel scoring system based on preoperative blood tests to predict the prognosis of atypical meningiomas, demonstrating the potential of integrating clinical and laboratory data for better patient outcomes (ref: Chen doi.org/10.3389/fonc.2020.01705/). Lastly, Wu et al. investigated the role of FOXM1 in malignant meningioma cells, revealing its promotion of tumor growth via the aryl hydrocarbon receptor signaling pathway, thus providing insights into potential therapeutic targets (ref: Wu doi.org/10.5114/fn.2020.100065/).