The concept of the so-called ‘vulnerable plaque’has proved highly useful to guide research and thinking regarding the pathophysiology of the acute coronary syndromes (ACS). Yet, the time may have come to reconsider this construct, as knowledge has accumulated, the risk profile of the populace has shifted, and our current therapies have reshaped the disease. Over the last several decades, the quest to identify and treat the ‘vulnerable plaque’has generated much interest. 1 Loaded with lipid, macrophage rich, covered by a thin fibrous cap, and considered perilously poised to rupture, the thin-capped fibroatheroma (TCFA) has become a target for imaging, possible intervention, model attempts in animals, and much discussion. 2 Many equate type 1 myocardial infarction with ‘plaque rupture’. Yet, the ‘vulnerable plaque’concept, as useful as it has proved heuristically, may not represent the contemporary challenge, an unmet clinical need, or a fertile field for future research.