Recent studies have elucidated the complex molecular mechanisms underlying IDH-mutant gliomas, particularly focusing on therapeutic targets and patient responses to mutant IDH inhibitors. One study profiled IDH-mutant oligodendrogliomas using single-cell RNA sequencing, revealing that patients who responded to IDH inhibitors exhibited distinct lineage differentiation patterns (ref: Spitzer doi.org/10.1016/j.ccell.2024.03.008/). Another significant finding highlighted a clinically aggressive subtype of IDH-mutant gliomas characterized by altered metabolism, which resembled IDH wild-type tumors, suggesting that metabolic profiling could inform treatment strategies (ref: Nassiri doi.org/10.1007/s00401-024-02713-1/). Furthermore, the identification of hypoxic macrophages in glioblastomas has opened avenues for therapeutic interventions aimed at normalizing tumor vasculature, indicating the potential for macrophage-targeted therapies in improving patient outcomes (ref: Wang doi.org/10.1016/j.ccell.2024.03.013/). In addition to these findings, the loss of methylthioadenosine phosphorylase (MTAP) expression was correlated with poor prognosis in glioma patients, with significant differences in progression-free survival (1.88 years vs. 6.80 years) and overall survival (5.23 years vs. 10.69 years) between MTAP loss and retention groups (ref: Yamamura doi.org/10.1007/s11060-024-04661-y/). Moreover, a feasibility study on advanced imaging techniques at 3T demonstrated the potential of various spin lock methods to differentiate between IDH and 1p/19q codeletion statuses, underscoring the importance of imaging in the molecular characterization of gliomas (ref: Jambor doi.org/10.1371/journal.pone.0296958/).