Restenosis after angioplasty has been recently attributed to a lack of compensatory enlargement and/or chronic constrictive remodelling, rather than neointimal growth. Also, restenosis occurring after stent has been clearly related to neointimal growth. This clarification has dramatically helped in designing strategies targeted against the appropriate mechanisms. The mechanism of stent-related restenosis has been the most studied and several antiproliferative agents including gene therapy and radioactive stents have been successfully tested. Constrictive remodelling has been identified more recently and its pathophysiological mechanism remains poorly understood. Control of extracellular matrix metabolism might be an important pathway. Moreover, detection of the arteries that will 'enlarge' should avoid any preventive strategy including systematic stenting.