Recent studies have elucidated various molecular mechanisms underlying glioblastoma, particularly focusing on glioblastoma stem cells (GSCs) and their interactions with the tumor microenvironment. Zhao et al. demonstrated that lymphatic endothelial-like cells (LECs) in glioblastomas promote the growth of CCR7-positive GSCs through the secretion of CCL21, highlighting the role of endothelial cell populations in tumor progression (ref: Zhao doi.org/10.1038/s43018-023-00658-0/). Additionally, Iser et al. introduced a molecular-guided tumor classification using cerebrospinal fluid (CSF) cfDNA sequencing, successfully identifying tumor entities in 75% of glioblastoma cases, which underscores the potential of CSF analysis in glioma diagnostics (ref: Iser doi.org/10.1158/1078-0432.CCR-23-2907/). Drexler et al. explored the temporal changes in DNA methylation subclasses between newly diagnosed and recurrent glioblastomas, revealing that subclass transitions correlate with metabolic process alterations and immune component variations, suggesting a dynamic tumor evolution (ref: Drexler doi.org/10.1007/s00401-023-02677-8/). Wang et al. further contributed to the understanding of glioblastoma metabolism by showing that genomic alterations influence CSF metabolite levels, indicating the clinical utility of CSF metabolite analysis (ref: Wang doi.org/10.1186/s40478-024-01722-1/). Lastly, Huang et al. investigated the role of the long non-coding RNA PVT1 in glioblastoma, finding that its expression promotes tumor proliferation and macrophage immunosuppressive polarization, thereby impacting the tumor microenvironment (ref: Huang doi.org/10.1111/cns.14566/).