Intimal hyperplasia (IH) is implicated in the pathogenesis of restenosis and is the main reason for treatment failure after revascularization procedures. One example of a strategy to reduce restenosis is the use of anti-inflammatory drugs such as paclitaxel, usually administered as a coating on a stent. Recently, the cell surface receptor Necl-5/CD-155 has been reported to be involved in VSMC proliferation and migration in vitro, and in VSMC de-differentiation and neointimal hyperplasia in vivo.