MET and melanoma: For example, EVs generated by highly metastatic melanoma cells can enhance the metastatic behavior of primary tumors by reprogramming bone marrow progenitors through the receptor tyrosine kinase Met, and induce vascular leakiness at pre-metastatic sites and reprogram bone marrow progenitors toward a pro-angiogenic phenotype dependent on c-Kit, the receptor tyrosine kinase Tie2 and Met [70].