In different tumor models (such as glioma, Lewis lung carcinoma, and spontaneous mammary carcinoma), treatment with an antibody that simultaneously activates Tie-2 and inhibits Ang-2 (ABTAA) was useful in restoring pericyte PDGFR-β coverage and tightening endothelial cell junctions by increasing VE-cadherin and claudin-5 expression, promoting the stabilization of pericyte–endothelial cell contact. This evidence concerns the gene TEK and neoplasm.