PTK2 and neoplasm: In particular, the pharmacological inhibition of FAK or its genetic ablation prevented the VEGF/vascular endothelial growth factor receptor-2 (VEGFR2)-dependent redistribution of FAK to the adherent junctions and the activation of both β-catenin and the vascular endothelial cadherin (VEC), then lowering the tumor cell migration across the endothelial barrier [170].