Percutaneous transluminal balloon angioplasty is currently the treatment of choice for obstructive atherosclerotic vascular disease. Still, more than 40% of initially successfully treated patients develop 'restenosis' within 6 months after the intervention, severely hampering the overall success of this therapeutic measure. The proposed mechanisms underlying the process of restenosis have led to respective therapeutic strategies ranging from the use of antiplatelet drugs and antioxidants to radiotherapy. None of the several strategies, however, could decrease the number of patients suffering from restenosis significantly. Inflammation has been implicated as an early step in the development of atherosclerosis and postangioplasty restenosis. The contribution of NFκB to restenosis could be demonstrated in animal experiments using adenoviral-based gene therapy overexpressing the inhibitor of NFκB, I-kB. This treatment resulted in significantly reduced inflammatory response, increased apoptosis, positive remodeling and significantly less lumen loss but no significant change in neointima formation. There is also a crosstalk between the NFκB pathway and the EGR-1/NAK-1 pathways. Modulation of the NAK-1/EGR-1 pathway resulted in reduced neointima formation but no lumen gain because of lack of positive remodeling.