A study using patient-derived liquid biopsy samples identified a tumor-derived miR-302/367 microRNA cluster carried in extracellular vesicles that can reprogram monocyte-derived macrophages toward an M2-like, immunoregulatory state in prostate cancer. Researchers reported that macrophage shifts tracked with histological grade in the diagnostic cohort. Functional experiments showed that inhibiting specific microRNAs within the cluster—miR-302a-5p and miR-367-3p—restored M1-like characteristics, while adding vesicles enriched with the microRNAs induced the M2-like program. The work suggested a mechanistic link between circulating tumor material and systemic myeloid conditioning. While the authors noted the study does not prove the microRNA activity drives grade progression, the findings create a pathway for potential clinical biomarker development or therapeutic targeting of the EV-miRNA signal.