SLC2A12 encodes GLUT12, an insulin-independent facilitative glucose transporter with broader metabolic roles than previously characterized. The protein functions as a plasma membrane glucose transporter mediating D-glucose transmembrane transport 1, but recent evidence reveals it also serves as a physiological urate transporter that regulates blood urate levels 2. SLC2A12 has emerged as a significant disease-associated gene across multiple pathologies. Genetic variants in SLC2A12 associate with primary open-angle glaucoma susceptibility across diverse ancestries 3 and myocardial interstitial fibrosis, implicating glucose transport dysfunction in cardiac fibrosis pathogenesis 1. In ovarian cancer, hypoxia upregulates SLC2A12 expression via HIF-1/HRE signaling, promoting tumor progression by suppressing ferroptosis through glutathione metabolism regulation; SLC2A12 silencing inhibits tumor growth and metastasis in vivo 4. Clinically, SLC2A12 shows diagnostic potential: plasma exosomal lnc-SLC2A12-10:1 is significantly upregulated in gastric cancer patients with superior diagnostic accuracy (AUC: 0.776) compared to conventional markers CEA, CA19-9, and CA72-4, correlating with tumor stage and metastasis 5. In intracranial aneurysm pathogenesis, SLC2A12 expression is downregulated in affected tissue and distinguishes aneurysms from controls 6. Promoter polymorphisms in SLC2A12 also associate with milk production traits in cattle 7.