Meningiomas, the most prevalent primary intracranial tumors, exhibit significant intratumor heterogeneity, which is crucial for understanding their molecular drivers and potential therapeutic targets. A study conducted multiplatform genomic profiling on 86 spatially distinct samples from 13 meningiomas, revealing mechanisms underlying this heterogeneity and identifying new molecular therapy targets (ref: Magill doi.org/10.1038/s41467-020-18582-7/). Another investigation focused on the sensitivity of meningioma cells to the cyclin-dependent kinase inhibitor TG02, finding that cell cultures from tumors assigned to a more malignant methylation class exhibited greater sensitivity, suggesting a potential link between methylation status and therapeutic response (ref: von Achenbach doi.org/10.1016/j.tranon.2020.100852/). Additionally, the identification of novel fusion transcripts in meningiomas, including six distinct fusion events, highlights the complexity of their genomic landscape and may provide insights into tumor biology and treatment strategies (ref: Khan doi.org/10.1007/s11060-020-03599-1/). High copy-number variation burdens were also noted in cranial meningiomas, with specific genomic regions correlating with clinical phenotypes, indicating that genomic alterations may influence tumor behavior and patient outcomes (ref: Ma doi.org/10.3389/fonc.2020.01382/). Proteomic analyses further elucidated signaling cascades in meningiomas, identifying druggable targets and pathways that could be exploited for therapeutic intervention (ref: Mukherjee doi.org/10.3389/fonc.2020.01600/). Lastly, a voxel-wise analysis of meningioma locations based on biological characteristics provided insights into tumor behavior and potential surgical implications (ref: Sun doi.org/10.3389/fonc.2020.01412/).