VEGFA and cancer: Studies by Al-Nedawi et al. 12 suggested that MVs shed by cancer cells expressing high levels of EGF receptors stimulated the expression of VEGF, giving rise to sustained signalling by endogenous VEGF from an endomembrane site (for example, endosomes), which could have important consequences given the suggestions that the endocytosis and localization of VEGFR2 to endosomes can play a key role in signalling to its downstream partners52, 53, 54.