The use of intracoronary stents has become the first choice of therapy in interventional cardiology. In most centers in the United States and Europe, stents are used in 70-80% of percutaneous coronary interventions.1,2 Although coronary stents reduce the incidence of restenosis compared to balloon angioplasty alone by opposing elastic recoil and late remodeling of the vessel,3,4 an excessive neointimal hyperplasia still induces in-stent restenosis in 10-30% of the patients.1 In-stent restenosis is a local, chronic response of the vessel wall to a foreign body, which involves a cascade of thrombotic, proliferative, and inflammatory phases.5 Many different cell types are recruited to play a pivotal role in this wound healing phenomenon: platelets, smooth muscle cells (SMCs), myofibroblasts, endothelial cells, and inflammatory cells (macrophages, lymphocytes, granulocytes, neutrophils). These cells release all kinds of growth factors which again stimulate the fibromuscular proliferative response of the vessel wall. The problem of in-stent restenosis is thus complex and therefore difficult to solve.