The data here support a major role of SLC26A3 in intestinal oxalate absorption, as diagrammed in Figure 5, and provide evidence for pharmacological inhibition of SLC26A3 as a potentially novel approach to reduce urinary oxalate excretion, with potential therapeutic benefits in enteric hyperoxaluria and calcium oxalate nephrolithiasis. The gene discussed is SLC26A3; the disease is nephrolithiasis susceptibility caused by SLC26A1.