Since one literature has revealed that PTEN could decrease the expression of CCL2 and VEGF-A to inhibit macrophage polarization from innate macrophages to M2 phenotypes in the tumor microenvironment 7, combined with our results, we conclude that exosomes containing Cav-1 could inhibit the PTEN/CCL2/VEGF-A signaling pathway to promote the M2 polarization and angiogenesis of lung macrophages, which may play an important role in the PMN formation and BC lung metastasis. This evidence concerns the gene CAV1 and breast cancer.