Recent GWAS identified genetic variants in urate transporters (ABCG2, SLC2A9, SLC22A11) and metabolic genes (GCKR, ADH1B) to be associated with the transition from hyperuricaemia to gout [10], and several of these associated with serum urate (SU) and gout in previous studies [11–15]. This evidence concerns the gene ADH1B and gout.