The activity of NF-kappa B is critically involved in the inflammatory activation of endothelial cells and their adhesiveness and also appears to regulate apoptosis in SMC by coordinating antiapoptotic programs. The activity of NF-kappa B has been revealed within human atheromas or following angioplasty but not in undiseased arteries. Hence, the inhibition of NF-kappa B mobilization by antioxidative or anti-inflammatory agents or by adenoviral I kappa B alpha overexpression, as reviewed herein, may act in concert to suppress endothelial activation and to induce SMC apoptosis. This synergistic concept may be a vasoprotective approach to prevent atherogenesis and restenosis by attenuating inflammatory reactions and SMC proliferation in nascent and progressing atherosclerotic lesions, as well as in developing neointima formations following angioplasty.