Tumor-derived EVs can transfer proangiogenic molecules into ECs to promote their angiogenic activity via various mechanisms such as VEGF/VEGF Receptor (VEGF/VEGFR), Notch, Wingless-type (WNT), and Hypoxia-inducible factor (HIF) signaling pathway (Phng et al., 2009; Horie et al., 2017; Todorova et al., 2017; Aslan et al., 2019). The gene discussed is VEGFA; the disease is neoplasm.