Gal-3 acts as an advanced glycation end products receptor, thus Gal-3's position on the emergence and advancement of long-term DM complications by its ability to bind advanced glycemic end products (AGEs) to advanced lip-oxidation end products (ALEs) which build up in the target organ and influence its toxic effects by causing pro-inflammatory and prooxidising pathways [9]. This evidence concerns the gene LGALS3 and diabetes mellitus.