In-stent restenosis reflects the interaction of a cascade of molecular and cellular events occurring within the vessel wall. Coronary stenting induces localized injury to the vessel wall, which leads to the release of thrombogenic, vasoactive, and lymphocytes mitogenic factors that result in processes causing re-narrowing at the injured site. Three major processes have been identified that lead to the in-stent restenosis: neointimal hyperplasia, elastic recoil, and negative arterial remodeling. The most important one is intimal hyperplasia. As the time course of neointimal hyperplasia is unknown, a causal relationship between the development of new blood vessels and clinical restenosis cannot be firmly established.