The principal aim of this study is to determine if molecular regulation of the human gene PAI-1 alters the migratory properties of human myeloid and endothelial cells sufficiently enough to regulate entry and exit from the vascular space. Human monocyte become the key cellular orchestrators of human atherosclerotic plaque. We believe that a "loss" of PAI-1 activity may promote a pro-atherogenic effect in human vasculature thereby defining a novel atheroprotective effect for PAI-1 when expressed at normal levels in humans. By using RNA interference to achieve PAI-1 gene, we hope to elucidate the mechanistic basis of how PAI-1 regulation may affect human migration within the vasculature.