In vitro and in vivo studies of SFs and synovial endothelium from patients with RA have shown enhanced expression of adhesion molecules, including E-selectin, vascular cell adhesion molecule VCAM-1, integrin α1β1 (VLA-1), intercellular adhesion molecule ICAM-1, or junctional adhesion molecule JAM-C, resulting from the abundant secretion of TNF-α, because a therapeutic blockade with monoclonal antibodies effectively reduces the expression of these molecules [25–31]. This evidence concerns the gene ICAM1 and rheumatoid arthritis.