Research on gliomas, particularly those with IDH mutations, has revealed critical vulnerabilities that can be targeted for therapeutic intervention. A study identified that IDH1-mutant glioma cells exhibit heightened sensitivity to inhibitors of the de novo pyrimidine synthesis pathway, particularly dihydroorotate dehydrogenase (DHODH), suggesting a potential therapeutic avenue for these aggressive tumors (ref: Shi doi.org/10.1016/j.ccell.2022.07.011/). Similarly, another investigation into diffuse midline glioma (DMG) highlighted a selective dependency on the de novo pyrimidine biosynthesis pathway, driven by oncohistone mutations, which could inform drug development strategies (ref: Pal doi.org/10.1016/j.ccell.2022.07.012/). The prognostic implications of surgical interventions in glioblastoma were also explored, with findings indicating that the classification system for extent of resection can significantly stratify patient outcomes, emphasizing the importance of removing non-contrast enhancing (non-CE) tumor tissue for improved survival rates (ref: Karschnia doi.org/10.1093/neuonc/). Furthermore, a national-level analysis of survival patterns for molecularly-defined diffuse glioma types revealed distinct overall survival outcomes based on molecular characteristics, underscoring the need for personalized treatment approaches (ref: Ostrom doi.org/10.1093/neuonc/). The incidence of pseudoprogression in IDH-mutant high-grade gliomas was also characterized, providing insights into diagnostic challenges and treatment responses in this patient population (ref: Seyve doi.org/10.1093/neuonc/).