With this respect, galectin-3 was shown to exert a protective effect toward the development of renal disease and atherosclerosis in experimental animal models [3, 4], that is, the opposite of the receptor for AGEs (RAGE), the first identified AGE receptor, which is known to mediate AGE/ALE-induced tissue injury [7] and to be upregulated in the absence of galectin-3 [3, 4]. This evidence concerns the gene LGALS3 and kidney disorder.