TGFBR3 and neoplasm: Vice versa, sEVs from M2-macrophages interacted with PDAC tumor cells as well as the extended TME, e.g., M2-derived sEVs with miR-501-3p inhibited transforming growth factor beta receptor 3 (TGFBR3), enabling TGF-β signaling, tumor growth, and metastasis of xenografted PDAC in nude mice.