In a recent study, Zhang et al. also showed that tumor B-cell-derived small EVs enriched with the ectonucleotidases CD39 and CD73 were able to hydrolyze ATP into adenosine, which is known to affect the cancer immune response, causing inhibition of post-chemotherapeutic CD8+ T-cell proliferation and cytotoxicity. The gene discussed is CD8A; the disease is neoplasm.