Considerable attention has been paid to the role of galectin-3 in the onset and progression of long-term complications of diabetes because of its ability to bind the advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs) that accumulate in target organs and exert their toxic effects by triggering proinflammatory and prooxidant pathways [5, 6]. This evidence concerns the gene LGALS3 and diabetes mellitus.