Meningiomas, the most prevalent primary brain tumors in adults, exhibit a complex interplay of genetic and molecular factors influencing their pathophysiology. Recent studies have focused on the molecular alterations associated with meningiomas, including the identification of somatic mutations and germline mutations that predispose individuals to these tumors. For instance, a study developed mouse models harboring mutations found in human meningiomas, confirming the role of specific genetic alterations in tumorigenesis (ref: Peyre doi.org/10.1056/NEJMoa2100440/). Another significant contribution is the proposal of a molecularly integrated grading system that aims to enhance the predictive power of clinical behavior beyond the traditional World Health Organization grading, which often fails to accurately reflect tumor aggressiveness (ref: Driver doi.org/10.1093/neuonc/). Furthermore, research into meningoangiomatosis, a rare condition linked to epilepsy, has revealed critical insights into the molecular landscape of these lesions, highlighting the need for comprehensive genetic profiling in clinical practice (ref: Dono doi.org/10.1093/jnen/). The exploration of germline BAP1 mutations in families with multi-generational meningiomas underscores the hereditary aspects of these tumors, particularly in aggressive rhabdoid variants (ref: Prasad doi.org/10.3389/fonc.2021.721712/). Lastly, innovative imaging techniques such as somatostatin receptor PET have been employed to assess tumor progression and receptor expression, providing valuable information for treatment planning (ref: Treglia doi.org/10.3390/diagnostics11091669/).