IDH-mutant gliomas exhibit significant molecular heterogeneity, necessitating a deeper understanding of their underlying mechanisms for improved therapeutic strategies. One study highlights the role of the PI3K/AKT/mTOR signaling pathway in driving disease progression in IDH-mutant diffuse gliomas, indicating that therapeutic inhibitors targeting this pathway could be beneficial (ref: Mohamed doi.org/10.1093/neuonc/). However, the prevalence of this pathway's activity remains unclear, and robust methods for assessing it in clinical samples are lacking. Another critical aspect is the chromosomal instability (CIN) observed in IDH-mutant astrocytomas, which has implications for tumor classification and patient management (ref: Liu doi.org/10.1186/s40478-022-01339-2/). This study emphasizes the need to integrate CIN into the molecular profiling of gliomas, as it may influence treatment decisions and prognostic assessments. Furthermore, research comparing IDH-mutant astrocytomas and oligodendrogliomas reveals distinct molecular features and immune microenvironments, suggesting that tumor purity could be a significant genomic factor affecting prognosis (ref: Zhao doi.org/10.1186/s10020-022-00454-z/). Lastly, a retrospective analysis of IDH1/2 mutations in glioma patients underscores the importance of combining immunohistochemistry (IHC) with massively parallel sequencing (MPS) to enhance mutation detection rates, particularly in younger patients (ref: Sporikova doi.org/10.1097/PAI.0000000000000997/).