Recent research has highlighted the critical role of the tumor microenvironment (TME) in the progression of neuro-oncological conditions, particularly glioblastoma. Kloosterman et al. demonstrated that macrophages facilitate the recycling of myelin-derived lipids, which are essential for meeting the high metabolic demands of glioblastoma cells, particularly in mesenchymal subtypes. This lipid transfer occurs via an LXR/Abca1-dependent mechanism, suggesting potential metabolic vulnerabilities that could be targeted for therapeutic interventions (ref: Kloosterman doi.org/10.1016/j.cell.2024.07.030/). In another study, Zhao et al. explored the role of the proto-oncogene c-SRC in glioblastoma progression, revealing that mutations in ACSS2 and ACLY significantly reduce fatty acid synthesis, thereby inhibiting tumor growth. This finding underscores the importance of fatty acid metabolism in glioblastoma malignancy and suggests that c-SRC inhibition could be a viable treatment strategy (ref: Zhao doi.org/10.1038/s41467-024-51444-0/). Furthermore, the immune landscape within gliomas has been characterized by Gupta et al., who utilized single-cell transcriptomics to identify distinct immune cell types and their contributions to glioma immunity, emphasizing the need for tailored immunotherapeutic approaches (ref: Gupta doi.org/10.1093/neuonc/). Together, these studies illustrate the intricate interplay between glioblastoma cells and their microenvironment, highlighting both metabolic and immune components as critical factors in tumor progression and potential therapeutic targets.