It promotes uric acid excretion by downregulating renal URAT1 and GLUT9 while upregulating ABCG2 and OAT1; simultaneously enhances intestinal excretion by upregulating intestinal ABCG2 and GLUT9; and regulates uric acid homeostasis through multiple pathways by inhibiting renal-intestinal inflammatory pathways, improving renal glucose metabolism disorders, and increasing beneficial bacterial abundance (Han et al., 2025). This evidence concerns the gene SLC2A9 and metabolic disease.