Baylis et al Implications of the CANTOS Trial for Vascular Biology e175 of plaque erosion and rupture vary, but even aggressive estimates suggest that rupture remains the primary driver of plaque failure. Indeed, a ruptured fibrous cap is found in approximately two-third of postmortem samples from patients dying of an acute coronary syndrome4 and intravascular imaging has shown that plaque rupture accounts for≈ 71% and 43% of ST-segment–elevation or non–ST-segment–elevation MI, respectively. 3 Although the PROSPECT study (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) showed that only 5% of thin-capped fibroatheromas resulted in a clinical event in 3.4 years, thin-capped fibroatheroma plaque morphology was the only independent risk factor that was predictive for a future event. 6 This latter observation emphasizes the point that major adverse cardiovascular events are relatively rare, but they are still much more likely to occur at high-risk thin-capped fibroatheromas. As an analogy, being struck by lightning may be an extraordinarily rare event, but it is still unwise to hold a metal rod in the air during a lightning storm. Both modes of lesion failure have critical clinical importance, and although it is suggested that over time erosion is becoming more prevalent as a pathological substrate of an acute MI, 3 it is too soon to write off rupture such that future studies of potential anti-inflammatory agents need to examine both of these processes.