In terms of pathological mechanisms, the notably increased mRNA expression levels of GLUT9, a uric acid reabsorption transporter, in the kidneys, along with the significantly elevated activities of XOD and ADA in the serum, as well as the significantly reduced mRNA expression levels of OAT1 and OAT3 in the kidneys, which are the primary uric acid secretion proteins, constitute the core pathological mechanism of hyperuricemia in our quail models. This evidence concerns the gene SLC22A8 and hyperuricemia.