VEGFA and neoplasm: This blockade leads to inhibition of new capillary formation by suppressing endothelial proliferation, migration and tube formation; reduction of VEGF‐A‐mediated autocrine survival signalling within tumour cells; induction of ‘vascular normalisation’, characterised by tightening of endothelial junctions, increased pericyte coverage, decreased vessel permeability, improved perfusion, alleviation of hypoxia and enhanced delivery and efficacy of concomitant therapies.16