Research in neuro-oncology has increasingly focused on the complex interactions between glioblastoma cells and their microenvironment, particularly the role of immune cells in tumor progression. A study utilizing single-cell RNA sequencing revealed that macrophages can induce glioblastoma cells to transition into mesenchymal-like states, which are associated with increased malignancy and therapeutic resistance (ref: Hara doi.org/10.1016/j.ccell.2021.05.002/). This finding underscores the importance of the tumor microenvironment in glioblastoma biology and suggests potential therapeutic targets to disrupt these interactions. Additionally, the efficacy of immunotherapy strategies has been explored, with dual targeting of IL-6 and CD40 showing promise in enhancing T-cell infiltration and improving survival outcomes in glioblastoma models (ref: Yang doi.org/10.1038/s41467-021-23832-3/). However, the challenge remains in overcoming the immunosuppressive tumor microenvironment, as indicated by the upregulation of prohibitin in glioma stem-like cells, which facilitates resistance to therapies by regulating mitochondrial reactive oxygen species (ROS) levels (ref: Huang doi.org/10.1038/s41467-021-24108-6/). Moreover, the recent updates to clinical guidelines regarding anticonvulsant prophylaxis in patients with newly diagnosed brain tumors emphasize a cautious approach, recommending against the routine use of antiepileptic drugs in patients without a history of seizures (ref: Walbert doi.org/10.1093/neuonc/). This reflects a growing recognition of the need for evidence-based practices in managing brain tumor patients. The identification of TERT promoter mutations as a critical diagnostic criterion for IDH-wildtype diffuse astrocytic gliomas further illustrates the evolving landscape of molecular diagnostics in neuro-oncology, with significant implications for prognosis and treatment strategies (ref: Fujimoto doi.org/10.1007/s00401-021-02337-9/).