Despite fifteen years of extensive research, we still do not know how to predict or prevent restenosis. Angioplasty induces lesions in the intima, media and sometimes adventitia, resulting in a cicatricial process comprising proliferation and migration of smooth muscle cells towards the intima and secretion of extracellular matrix, leading to the formation of a neointima. Since angioplasty is associated with the simultaneous development of neointimal hyperplasia and restenosis, a cause and a effect relationship has therefore been proposed between neointimal hyperplasia and restenosis. All the restenosis prevention strategies based on inhibition of smooth muscle cell proliferation, which successfully limited restenosis in animal models have failed in man, due to the hazardous extrapolations from experimental models which are very different from the atheromatous lesions observed in man, rather than to the use of animal models in general. It is reasonable to wonder whether we have not selected the wrong target: is smooth muscle cell proliferation really responsible for restenosis? Experimental results supported by histological and ultrasonographic data in man, show that the cicatricial process which induces restenosis consists of constrictive remodelling, which decreases the perimeter of the external elastic lamina and the lumen. The use of stents appears to be the primary strategy designed to limit restenosis and prevent constrictive remodelling in man, even if it stimulates neointimal hyperplasia. Progress in the understanding of the mechanisms of postangioplasty remodelling open new perspectives in the prevention of restenosis.