Our data on Exos-dependent endothelial cell expression of EGFR, its phosphorylation and Gefitinib-dependent inhibition of Exos-induced capillary morphogenesis (Fig. 6) are supported by several evidences that stimulation or inhibition of EGFR has significant consequences on tumor angiogenesis, a feature that involves both a direct effect and an interplay with VEGF [47–51]. The gene discussed is EGFR; the disease is neoplasm.