SLC17A4 is a membrane transporter with multiple critical functions in anion and thyroid hormone homeostasis. As a membrane potential-dependent organic anion transporter, it mediates chloride-dependent urate transport and sodium-independent phosphate uptake via Na+ cotransport 1. SLC17A4 functions as a high-affinity thyroid hormone transporter, facilitating the cellular uptake and efflux of both T3 and T4 in a sodium- and chloride-independent manner that is stimulated by low extracellular pH 2. It also transports reverse T3 and 3,3'-diiodothyronine, though less efficiently 2. The transporter undergoes N-linked glycosylation, which is essential for its function 2. Clinically, SLC17A4 has emerging disease relevance across multiple conditions. Genetic variants in SLC17A4 associate with altered circulating free T4 concentrations and thyroid dysfunction affecting ~10% of the general population 34. SLC17A4 variants also contribute to gout progression from hyperuricemia 5 and were identified as iron-related biomarkers in chr6 rhinosinusitis, with reduced SLC17A4 expression correlating with disease severity 6. Additionally, SLC17A4 knockdown inhibits prostate cancer cell proliferation and invasion 7, and SLC17A4 methylation changes associate with gestational diabetes mellitus exposure in offspring 8.