SLC26A6 is a multifunctional anion transporter expressed in kidney, intestine, pancreas, and other organs that mediates electroneutral chloride-bicarbonate exchange and electrogenic chloride-oxalate exchange 1. The transporter operates at the apical membrane and associates with carbonic anhydrase CA2 to form a bicarbonate transport metabolon, optimizing local bicarbonate concentration [UniProt annotation]. SLC26A6 also transports sulfate and other anions, playing crucial roles in intestinal anion absorption, renal oxalate homeostasis, and acid-base regulation 2. In renal physiology, SLC26A6 mediates transcellular proximal tubule chloride reabsorption and intestinal back-secretion of oxalate 2. Dysfunction of SLC26A6 leads to hyperoxaluria and calcium oxalate nephrolithiasis; notably, Slc26a6 null mice develop urolithiasis due to impaired intestinal oxalate secretion 2. Recent evidence demonstrates that unconjugated bilirubin upregulates Slc26a6 expression, increasing renal oxalate secretion and promoting calcium oxalate crystal deposition 3. SLC26A6 mutations cause enteric hyperoxaluria and stone formation in patients 1. Beyond renal disease, SLC26A6 is implicated in hepatocellular carcinoma pathogenesis, where elevated expression correlates with poor prognosis and associates with PI3K-AKT signaling pathways 4. SLC26A6 dysfunction also contributes to intestinal, pancreatic, skeletal, and cardiac pathologies 5.