Likewise, EVs derived from highly metastatic melanomas that contain high levels of the receptor tyrosine kinase c-met increased the number of distant melanoma metastases (e.g., in bone and lung) compared with those released from a poorly metastatic melanoma cell line [4]; the mechanism advocated consisted of the influence or “education” of bone marrow progenitor cells through the horizontal transfer of the EV-associated phosphorylated c-met to PMNs and/or an increase in vascularization [4]. The gene discussed is NTRK1; the disease is melanoma.