These different biochemical and clinical characteristics may represent the substrate for a different evolution of the atherosclerotic process in patients with T2DM and DMC, with underlying mechanisms mainly related to the injurious effects of hyperglycaemia and insulin therapy (i.e., oxidative stress, endothelial dysfunction, low-grade inflammation, rheological abnormalities and fibrosis activation) [26–28]. Here, INS is linked to Dyggve-Melchior-Clausen disease.