Risk factors for atherosclerosis, including diabetes, have been identified for many years, and, especially for lipids, we now know a great deal about how these factors contribute to the early lesion. In contrast, the mechanism or mechanisms linking these factors to the final events in atherosclerosis, that is plaque rupture and thrombotic occlusion, have remained largely speculative. This speculation has been because of a lack the ability to visualize fragile, advanced lesions in humans and a lack of animal models. Recently, however, magnetic resonance imaging tools have begun to visualize the advanced lesion and animal models with features of plaque rupture have been characterized. Thus the opportunity exists to test hypotheses linking diabetes to events in the advanced plaques. This review summarizes our current knowledge of the processes that may be responsible for increased plaque rupture and occlusion associated with diabetes.