Recent studies have significantly advanced our understanding of the genetic and molecular underpinnings of meningiomas, particularly focusing on clear cell meningioma (CCM) and its association with SMARCE1 deficiency. St Pierre et al. demonstrated that the loss of SMARCE1, a crucial component of the mammalian SWI/SNF chromatin remodeling complex, leads to a dependency on the canonical BAF complex, suggesting potential therapeutic targets for CCM (ref: St Pierre doi.org/10.1038/s41588-022-01077-0/). Furthermore, Ferreyra Vega et al. highlighted the intratumor genetic and epigenetic heterogeneity in both diffuse gliomas and meningiomas, emphasizing the need for tailored clinical diagnostics that consider this variability (ref: Ferreyra Vega doi.org/10.1038/s41379-022-01113-8/). Walsh et al. explored genetic pleiotropy, identifying a meningioma risk locus on chromosome 10p12 that overlaps with loci associated with breast and ovarian cancers, indicating shared hormonal risk factors among these tumor types (ref: Walsh doi.org/10.1093/noajnl/). Additionally, Fu et al. investigated the role of M2 macrophage-derived exosomes in promoting meningioma progression, revealing a novel pathway that underscores the importance of the tumor microenvironment in meningioma biology (ref: Fu doi.org/10.1155/2022/). Lastly, a scoping review by Palmisciano et al. examined the use of cesium-131 brachytherapy in brain tumors, including meningiomas, highlighting its potential to minimize complications while maximizing treatment efficacy (ref: Palmisciano doi.org/10.1007/s11060-022-04050-3/).