Stents have been shown to reduce the incidence of restenosis; however, they are not a cure. In two trials the angiographic restenosis rate was reported to be between 20% and 30% (in the Benestent II trial the unpublished quoted restenosis rate was 15%). These trials were based on stenting short, de novo lesions, in native coronary arteries. Whether such results are applicable to the widespread stenting that is currently being practised is not clear. It has been shown that the incidence of in-stent restenosis may vary according to the conditions of stenting and the vessel being stented. The number of stents deployed, whether there has been previous intervention, the size of vessel stented, the location of the lesion, whether the vessel is a native coronary artery or vein graft, co-morbid conditions such as diabetes, and stent design may all affect the incidence of in-stent restenosis. Rates of up to 40% have been reported when lesions other than de novo Benestent-type are treated. How factors such as multiple stenting promote restenosis is not always clear. The next goal in stent development therefore should be to reduce further the need for repeat intervention for any stent deployed under any circumstance. Stents prevent negative remodelling and recoil. The need for repeat intervention is predominantly because of tissue ingrowth. Extensive animal data and information from some human postmortem samples have identified the nature of in-stent restenosis. The process appears to be initiated by a giant cell based inflammatory reaction centred on the stent struts (fig 1).1 Thereafter the responses to the stent are similar to many of the changes demonstrated previously for balloon angioplasty. Smooth muscle cells migrate through the internal elastic lamina and proliferate in the newly formed intimal layer (fig 2).2 Angiographic studies and intravascular ultrasound suggest stents …