Angiogenesis is stimulated by vascular endothelial growth factor (VEGF) which induces the openings between the cell junctions and the migration of precursor endothelial cells to form the lining of a new blood vessel [27] and it’s known that macrophages release VEGF when they adapt to the tumor microenvironment [28], hence we wondered if the circulating EVs of MM patients (pre- and post-treatment) could modulate the release of this factor. The gene discussed is VEGFA; the disease is neoplasm.