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Clearly, macrovascular complications are the prognosis limiting problem of diabetes patients which consecutively account for the majority of socio-economic burden of the disease. The overall morbidity and mortality development does not indicate improvement hallmarking better or at least adequate care for these patients. Possible explanations address the late detection problem of a clinically silent disease onset as well as unrecognised multiple comorbid conditions all of which end-up with endothelial dysfunction as representation of the so called "functional atherosclerosis" and blood hyperresponsiveness. Here, we describe new experimental aspects of the early atherosclerosis development focussing inflammation as one driving pathogenetic force for the evolution of the complicated lesion type in diabetes. However, emphasis is put on the view that inflammation, atherogenesis and thrombogenesis are severely crosslinked by soluble and cellular adhesion molecules. From a diagnostic point of view genomic detection of risk associated genes opens both the vision of early identification of high risk individuals and the targeting of drug intervention based on conditioned responsiveness. By using available drugs and evidence based risk factor intervention strategies a plea is made for a multimodal therapeutic approach fitted to the individual patient's needs aiming at endpoint reduction. This corresponds to the recent releases of guidelines from nearly all vascular medicine related scientific societies. Diabetes is a vascular disease!