These data suggest that functional and organic damage of media layer smooth cells in SS may be determined by a cellular infiltration of subendothelial space and the increased serum levels of adhesion molecules, such as ICAM-1 and VCAM-1, detected in SS patients may support that upregulation of these molecules on endothelial layer facilitates leukocyte infiltration within arterial wall with subsequent induction of atherosclerotic damage (38). This evidence concerns the gene VCAM1 and synovial sarcoma.