In T2DM and the metabolic syndrome, factors other than hyperglycemia, including changes in the inflammatory milieu associated with obesity, are likely to prevent normal atherosclerosis regression, and the versatile approach afforded by HDAd-LDLR treatment will make possible insightful investigations of these and other dysmetabolic settings. This evidence concerns the gene LDLR and obesity due to melanocortin 4 receptor deficiency.