For instance, EVs derived from cancer cells overexpressing a wild-type EGFR can result in angiogenesis by transferring the receptor to nearby endothelial cells and promoting their vascular endothelial growth factor (VEGF) expression, the latter can further induce activation of the key signaling receptor (VEGF receptor-2) in an autocrine manner [15]. The gene discussed is VEGFA; the disease is cancer.