In-stent restenosis is set to become a large part of our interventional practice in the new millennium. Stent implantation has grown so much that it now comprises 60–70% of all percutaneous coronary revascularisation interventions, and assuming a conservative 25% restenosis rate for a total of around one million percutaneous transluminal coronary angioplasty (PTCA) procedures this year, more than 150 000 lesions will need treatment because of in-stent restenosis. The increasing popularity of stent implantation is because of improvements in immediate gain, in tackling dissections, in preventing recoil after PTCA, and in reducing late restenoses, which have been documented in many randomised trials where results have been compared with PTCA. However, despite excellent immediate results, stents have not eliminated restenosis, especially in complex lesions with diffuse coronary disease or in small vessels.1-4 Furthermore, the mechanism of in-stent restenosis is very different from that of restenosis after conventional percutaneous treatment (PTCA, directional, rotational, or laser atherectomy). Lumen narrowing after these latter interventions is mainly caused by late wall recoil, and this negative remodelling of the treated segment can easily be treated with a new PTCA or by stent implantation.5 ,6 The stent, on the other hand, maintains the expansion it reaches after the procedure and all the reduction in lumen diameter is caused by intimal hyperplasia.7 The challenge to the interventionist in the coming years is how to prevent and treat this condition. Recently the Washington group suggested an angiographic classification of in-stent restenosis according to lesion length and geographical distribution of intimal hyperplasia in relation to the implanted stent. Four patterns of in-stent restenosis were suggested (table 1), with different impacts on the late outcome after a new revascularisation procedure.8