Intriguingly, gout patients exhibit reduced BA synthesis and altered BA pools (20, 21), suggesting that BA dysmetabolism may orchestrate gout progression through multiple mechanisms: 1) Uric acid (UA) metabolism: BAs inhibit hepatic xanthine oxidase (XOD) via proliferator-activated receptor alpha (PPAR-α), reducing urate production; their deficiency exacerbates hyperuricemia (22). This evidence concerns the gene XDH and hyperuricemia.