The ability of lactacystin to specifically and irreversibly bind the proteasome sparked research interest in its therapeutic potential for inflammatory diseases involving the UPS, such as atherosclerosis.68 In a study characterizing the role of endothelium-dependent mechanisms in pathological leucocyte transmigration, Allport et al.65 demonstrated that treatment with lactacystin inhibited surface expression of E-selectin, ICAM-1, and VCAM-1 and functionally suppressed inflammatory adhesion and transmigration of human neutrophils with HUVECs. This evidence concerns the gene VCAM1 and atherosclerosis.