The results of our previous study showed that sEVs from BC function as a signaling molecule to mediate intercellular communication and regulate the PMN prior to lung metastasis by controlling the expression of PMN marker genes and inflammatory chemokines in lung epithelial cells, encouraging the release of tenascin-C (TnC) in lung fibroblasts to cause the deposition of extracellular matrix (ECM), and inhibiting the PTEN/CCL2/VEGF-A signaling pathway in lung macrophages to facilitate their M2-type polarization and angiogenesis 18. The gene discussed is CCL2; the disease is breast cancer.