Obviously, owing to the evolutionary inactivation of Uox in humans, genetic modification of rodent Uox is an essential and most effective way to replicate human hyperuricemia and urate biology, as compared to genetically engineered mice targeting other loci (for example, SLC2A9 and ABCG2), as well as environmentally induced models [9, 11–13]. This evidence concerns the gene SLC2A9 and hyperuricemia.