Drug eluting stents (DES) have attracted considerable attention due to concerns of late stent thrombosis (LST) thought to be related to delayed endothelialisation. This hypothesis is based on clinical autopsy studies indicating an association between lack of endothelium and LST. However, meta-analysis of clinical trials does not support the notion that all DES induce more late stent thrombosis than BMS. In addition, preclinical data using animal models also do not necessarily support this hypothesis. Most animal models using single non-overlapping stents show no signs of delayed endothelialisation at all. Experiments with several DES in our laboratory using the porcine coronary artery model also suggest that DES show no differences in re-endothelialisation. They can however induce (late) differences in endothelial function, depending on the DES of choice. These phenomena are also described clinically in coronary segments distal from the DES. We hypothesise that DES do not necessarily delay endothelialisation but more likely induce late endothelial dysfunction that varies between DES.