The study demonstrated that VEGF promotes tension-independent FAK activation, FAK localization to endothelial adherent junctions, binding of the FAK FERM domain to VE-cadherin, and direct FAK phosphorylation of β-catenin on Y142 residue, causing disassembly of junctions, supporting vascular permeability and tumour cell extravasation [45]. The gene discussed is PTK2; the disease is neoplasm.