Given the pleiotropic roles played by VEGF and its receptor in RA inflammation [2, 3, 8, 24], it can be postulated that anti-VEGF treatment retards chronic synovitis in several ways, as follows: (a) it may decrease nutrient supply to the tumor-like synovium; (b) inhibit leukocyte adhesion and migration by decreasing endothelial cell surface area; (c) decrease chemokine and cytokine productions by activated endothelial cells; (d) reduce the VEGF-induced productions of TNF-α and IL-6 by monocytes/macrophages; (e) abrogate VEGF-induced increases in synoviocyte survival. Here, TNF is linked to rheumatoid arthritis.