Tumor cell-derived EVs participate in tumor cell proliferation in an autocrine/paracrine manner; for example, chronic myeloid leukemia (CML)-derived EVs contain large amounts of TGF-β1, which activates the ERK, Akt, and NF-κB pathways by binding to the TGF-β1 receptor on the surface of CML cells. The gene discussed is TGFB1; the disease is neoplasm.