Late stent thrombosis (ST) made headlines when investigators realized that clinical events related to late ST, although rare, carried a mortality rate of up to 45% and a nonfatal infarction rate of another 30% to 40%.1,2 These rates clearly were more than those seen after bare metal stent (BMS) implantation, as first shown prospectively in the randomized Basel Stent Kosten Effektivitats Trial–Late Thrombotic Events (BASKET-LATE).2 This led to a “firestorm,” which cooled off in view of the facts that these rare events are counterbalanced to some extent by fewer restenosis-related events in patients treated with drug-eluting stents (DES) versus BMS2,3 and that results of meta-analyses of earlier randomized trials4 and findings of large registries showed no overall excess mortality after DES versus BMS. Still, after DES implantation, late ST does occur, later than after BMS, at a relatively constant rate over time up to at least 4 years after stenting5 and, unlike after BMS, appears as primary thrombosis with a sudden unexpected clinical event not related to repeat interventions. Autopsy studies showed that delayed healing, ie, the lack of incomplete endothelial coverage of stent struts associated with persistence of fibrin deposits, is the primary pathoanatomic substrate of late ST after DES implantation.6 This was not found in patients with BMS. Delayed healing is the mechanism for late ST, ie, ST after 30 days of stent implantation, which was confirmed by intravascular ultrasound7 and angioscopic studies,8 and is quite different from early ST. Here, procedural factors such as incomplete lesion coverage, plaque protrusion, and persistent dissection represent the most important reasons for thrombosis. For late ST, additional risk factors such as incomplete stent apposition, very long stented segments, and bifurcation stenting have been recognized. Still, questions remained regarding the large number of “off-label” …