SLC2A9 encodes GLUT9, a high-capacity urate transporter primarily responsible for urate reabsorption in proximal tubule cells 12. The transporter demonstrates markedly greater affinity for urate than glucose, with urate transport rates 45-60 fold faster than glucose 3. While SLC2A9 retains residual glucose and fructose transporter activity, it does not transport galactose or most nucleobases 4. SLC2A9 functions alongside URAT1 (SLC22A12) and ABCG2 to regulate serum urate levels, which critically determines gout susceptibility 15. Genetic variations in SLC2A9 significantly influence gout risk; meta-analyses identified four SNPs associated with disease, with rs3733591 increasing gout susceptibility in Asians, while rs16890979 and rs1014290 provide protection across populations 6. Loss-of-function SLC2A9 mutations cause renal hypouricemia type 2 (OMIM 612076), an autosomal recessive disorder characterized by severely reduced serum urate and increased urinary excretion 7. Beyond urate homeostasis, SLC2A9 polymorphisms associate with oral microbiota composition, suggesting broader physiological roles 8. These findings establish SLC2A9 as a major genetic determinant of plasma uric acid levels and gout development, with therapeutic implications for urate-lowering strategies.