Recent studies have highlighted the complex role of extracellular vesicles (EVs) in cancer biology, particularly in the context of tumor progression and immune evasion. One study demonstrated that glucose restriction can paradoxically promote lung metastasis in cancer by depleting natural killer (NK) cells through macrophage-mediated mechanisms, with exosomal TRAIL playing a crucial role in this process (ref: Wu doi.org/10.1016/j.cell.2025.06.027/). Another investigation into non-small cell lung cancer (NSCLC) revealed that subclonal variations within tumors can significantly impact immune escape, suggesting that the genetic diversity of tumors must be considered when developing immunotherapies (ref: Dijkstra doi.org/10.1016/j.ccell.2025.06.012/). Furthermore, combining pembrolizumab with radiotherapy was shown to induce systemic antitumor immune responses in immunologically cold NSCLC, leading to improved progression-free survival, indicating that EVs may mediate the immunomodulatory effects of such treatments (ref: Huang doi.org/10.1038/s43018-025-01018-w/). Additionally, circRNA circERC1 was identified as a key player in chemoresistance in pancreatic cancer, suggesting that EVs can influence the tumor microenvironment and treatment outcomes (ref: Zhang doi.org/10.1186/s12943-025-02385-9/). Overall, these findings underscore the multifaceted roles of EVs in cancer biology, from mediating immune responses to influencing treatment resistance.