Clinically, the most common causes of hyperuricemia are insufficient excretion of UA in the kidney, downregulation of UA secretion transporter (urate-anion transporter 1 (URAT1), glucose transporter 9 (GLUT9), et al.)[15,16] and up-regulation of reabsorption transporter (ATP-binding cassette super family G number 2 (ABCG2), organic anion transporter 1 (OAT1), sodium-dependent phosphate cotransporter 1 (NPT1), et al.)[17,18,19]. Here, ABCG2 is linked to hyperuricemia.