Extracellular vesicles (EVs) derived from tumors play a pivotal role in cancer therapy, particularly in modulating immune responses and tumor microenvironments. A study demonstrated that tumor-derived extracellular vesicles (TEVs) often express immuno-evasive ligands like CD47, which inhibit phagocytosis by dendritic cells and macrophages, thereby facilitating tumor survival (ref: Ding doi.org/10.1038/s41565-024-01783-2/). This finding underscores the importance of engineering TEVs to mask these ligands, enhancing the efficacy of tumor vaccination strategies. Additionally, research revealed that EVs containing acyl-CoA synthetase long-chain family member 4 (ACSL4) from hepatocellular carcinoma cells can induce senescence in hepatocytes, promoting a tumor-supportive microenvironment (ref: Hou doi.org/10.1158/0008-5472.CAN-24-0832/). Furthermore, melanoma-derived EVs were shown to convert normal dermal fibroblasts into carcinoma-associated fibroblasts through miR-92b-3p-mediated PTEN downregulation, highlighting the role of EVs in tumor progression (ref: Kewitz-Hempel doi.org/10.1002/jev2.12509/). These studies collectively illustrate the dual role of EVs in both promoting tumor growth and serving as potential therapeutic targets in cancer treatment. Moreover, engineered EVs containing MAP kinase kinase 1 (MEK1) have been shown to enhance anti-tumor immunity, suggesting a promising avenue for future immunotherapeutic strategies (ref: Searles doi.org/10.1002/jev2.12515/).