Extracellular vesicles (EVs) play a critical role in cancer biology, particularly in the context of metastasis and immune evasion. Lucotti et al. demonstrated that small extracellular vesicles (sEVs) secreted by CXCL13-reprogrammed interstitial macrophages in the lung microenvironment contribute to cancer-associated thrombosis and metastasis, highlighting the significance of the pro-thrombotic niche in multiple cancers (ref: Lucotti doi.org/10.1016/j.cell.2025.01.025/). In a contrasting study, Freitas-Cortez et al. explored how cancer cells evade ferroptosis, a form of cell death induced by immune cells, by upregulating fatty acid binding proteins, thus allowing tumors to resist immune-mediated attacks (ref: Freitas-Cortez doi.org/10.1186/s12943-024-02198-2/). This underscores the complex interplay between cancer cells and the immune system, where EVs can either facilitate tumor progression or serve as mediators of immune responses. Furthermore, Ma et al. found that tumor-derived PD-L1 in EVs promotes T cell senescence through lipid metabolism reprogramming, suggesting that EVs can modulate immune cell functionality and contribute to the challenges faced in cancer immunotherapy (ref: Ma doi.org/10.1126/scitranslmed.adm7269/). The studies collectively emphasize the dual role of EVs in cancer, acting as both facilitators of tumor progression and potential targets for therapeutic intervention.