Intracoronary stents became the standard of care for the treatment of obstructive coronary artery disease following their approval by the US FDA in 1994. Stenting was especially successful for the treatment of early complications, such as sudden collapse of the artery and dissections, which were common following the use of balloon angioplasty on its own. Although there has been an improvement, this technology still had its limitations, namely a high incidence of recurrent luminal obstruction (restenosis) in at least 30–40% of individuals. Preclinical and clinical studies documented the importance of strut thickness and design of stents. However, none of the modifications appreciably reduced the incidence of in-stent restenosis. Many systemic and local drug therapies were successful at reducing intimal formation in animals but failed to show benefit in humans. There followed a period of a decade of a ‘love affair’with intravascular pharmacotherapy and brachytherapy, with success in the latter but late stent thrombosis and restenosis occurring as a complication. Then, in 2004, came the current era of drug-eluting stents (DESs), involving stent-based delivery of antiproliferative agents, which reduced restenosis rates dramatically in clinical trials without significant adverse effects and became the standard of care for the percutaneous treatment of coronary artery disease. However, the acceptance proved to be overly enthusiastic after several case reports raised concerns about an increased risk of late stent thrombosis (LST). In Barcelona (Spain) in 2006, a presentation at the European Society of Cardiology (ESC) by Camenzind ignited a ‘firestorm’with report of increased late stent thrombosis in the Cypher™(Cordis Johnson & Johnson Corp., FL, USA) clinical program, which reported an increase in all-cause death versus bare-metal stents (BMS), whereas the Taxus™(Boston Scientific, MA, USA) program only reported adjudicated cardiac death. Statistical differences were observed between DESs and BMSs for myocardial infarction and death but could only be documented in the Cypher and not for the Taxus program. Again in Barcelona, 3 years later (2009) at another ESC meeting, another session was organized to discuss ‘Is it time to turn the page on Barcelona 2006?’The speakers included Camazind, Kastrati and James. Camazind presented a study demonstrating an enduring risk of LST of 0.6 per year and accumulative incidence of 3.3% at 4-year follow-up, whereas Kastrati emphasized that all DESs are effective in reducing restenosis with reductions in repeat revascularization and no increase in LST. James from Uppsala Clinical Research Center, Sweden, on the Swedish Coronary Angiography and Angioplasty Registry (SCAAR) declared that ‘SCAAR scare’is no more; however, he stated that the Achilles heel of DESs remains stent thrombosis. Therefore, controversies remain and we need to look into the future and determine how can we improve DESs and what steps have already been taken by the industry and what new technology can be applied for the long-term safety of DESs.