Interestingly, phosphorylation of VEGFR2 at the Y949 residue (pY949) in mice (pY951 in humans) enables Src phosphorylation at Y416 and subsequently dissociates the VEGFR2/VE-cadherin/Src complex at endothelial junctions to decrease tumor vascularization and growth and increase vascular permeability [19, 21]. This evidence concerns the gene SRC and neoplasm.