Furthermore, Tat could enhance endothelial dysfunction through endothelial cell expression of various adhesion molecules, including soluble intracellular adhesion molecule (ICAM-1) and soluble vascular cell adhesion molecule (VCAM-1) [41, 42], possibly by potentiating the TNF-mediated activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [42]. The gene discussed is TNF; the disease is endothelial dysfunction.