Recent studies have significantly advanced our understanding of the molecular and genetic landscape of meningiomas, particularly focusing on specific subtypes and their unique characteristics. For instance, a study identified clear cell meningiomas as a distinct molecular subset characterized by a unique DNA methylation profile and frequent mutations in the SMARCE1 gene, highlighting the importance of genetic screening in this rare variant (ref: Sievers doi.org/10.1007/s00401-020-02247-2/). Another investigation into the Tübingen meningioma cohort revealed that loss of H3K27me3 trimethylation is associated with a higher risk of tumor recurrence, suggesting that this epigenetic marker could serve as a valuable prognostic tool in clinical settings (ref: Behling doi.org/10.1093/neuonc/). Furthermore, research on neurofibromatosis type 2 (NF2) patients indicated that those asymptomatic at diagnosis had better survival outcomes compared to symptomatic individuals, emphasizing the need for early detection and monitoring strategies (ref: Forde doi.org/10.1093/neuonc/). Additionally, the efficacy of decitabine in malignant meningioma cells was explored, revealing its potential to demethylate tumor suppressor genes and affect cell viability, independent of TERT expression (ref: Stögbauer doi.org/10.3171/2020.7.JNS193097/). Whole-exome sequencing studies have also uncovered overlapping genetic variants in blood, tissues, and cell lines from meningioma patients, predominantly in stem cell-related genes, which may provide insights into tumorigenesis and progression (ref: Hussein doi.org/10.1016/j.heliyon.2020.e05632/).