In conclusion, we found that pharmacological inhibition of colonic anion exchanger SLC26A3 by a selective, small-molecule inhibitor was effective in reducing intestinal oxalate absorption and preventing renal calcium oxalate deposition and injury in animal models of hyperoxaluria, supporting its potential utility as a first-in-class therapy for enteric hyperoxaluria and calcium oxalate nephrolithiasis. The gene discussed is SLC26A3; the disease is Hyperoxaluria.