In the light of the salient functions of CCL2 as a chemokine, combined with its association with endothelial dysfunction and disruption of the BBB, it would be of interest to examine if the enhanced CCL2 response from EC following CS-Tat treatment would also translate into an altered expression of lymphocyte, monocyte, or endothelial cell surface adhesion molecules and increased expression of Matrix metalloproteinases (MMPs). The gene discussed is CCL2; the disease is endothelial dysfunction.