SLC26A1 encodes a sodium-independent anion transporter that serves as a major determinant of sulfate homeostasis in humans 1. The protein functions as a versatile anion exchanger, mediating sulfate transport and facilitating anion exchange with bicarbonate, thiosulfate, and oxalate 2. SLC26A1 is predominantly expressed in kidney and liver, with the encoded protein containing 12 putative transmembrane domains 2. Loss-of-function variants cause hyposulfatemia and hypersulfaturia, demonstrating the transporter's critical role in renal sulfate reabsorption 1. The gene is associated with calcium oxalate nephrolithiasis, as Slc26a1-knockout mice develop hyperoxaluria and kidney stones 3. Clinical significance includes associations with musculoskeletal disorders, as sulfate is essential for bone and cartilage health 1. Human genetic studies have identified damaging SLC26A1 variants in patients with recurrent calcium oxalate stones and painful perichondritis 41. Population-level analyses confirm that rare damaging variants are associated with lower plasma sulfate levels and increased risk of musculoskeletal abnormalities 5. The transporter may also play roles in hepatic detoxification pathways, as knockout mice show increased susceptibility to acetaminophen-induced liver injury 6.