By elucidating a TEVs-mediated activation mechanism of TGF-β/SMAD signaling in recipient cells, we have revealed a TEVs-dependent cancer progression mechanism, via which tumor cells can not only become more malignant but also become more repressive to the antitumor immunity, and for which TβRII seems to be the first breast cancer extracellular vesicles marker identified. The gene discussed is TGFBR2; the disease is neoplasm.