Recent studies have significantly advanced our understanding of the molecular and genetic landscape of meningiomas, the most common primary intracranial tumors. Prager et al. explored the enhancer landscape of 33 meningioma tumors, identifying three distinct biological subgroups characterized by their hormonal lineage transcriptional regulators: adipogenesis/cholesterol, mesodermal, and neural crest. This stratification not only provides insights into tumor biology but also highlights potential druggable dependencies, paving the way for targeted therapies (ref: Prager doi.org/10.1158/2159-8290.CD-20-0160/). Sievers et al. further contributed to this theme by demonstrating that homozygous deletions of CDKN2A/B are associated with early recurrence in meningiomas, emphasizing the importance of genetic alterations in predicting clinical outcomes (ref: Sievers doi.org/10.1007/s00401-020-02188-w/). Additionally, Findakly et al. investigated the role of primary cilia in meningioma cells, revealing that while these tumors express primary cilia, they do not transduce Hedgehog signals, which are crucial for cellular signaling and development (ref: Findakly doi.org/10.1186/s40478-020-00994-7/). This suggests a unique aspect of meningioma biology that may influence therapeutic strategies. Zheng et al. identified a polymorphism in the MALAT1 gene that modulates meningioma invasiveness through its interaction with collagen type V alpha, further illustrating the complex genetic interplay in tumor behavior (ref: Zheng doi.org/10.1111/jcmm.15637/).