The potential pathophysiologic mechanisms of obesity-induced hyperoxaluria might be as follows [13–16]: (a) increased intake of oxalate and increased oxalate intestinal absorption daily; (b) obese subjects had decreased number of Oxalobacter formigenes, which could degrade intestinal luminal oxalate and stimulate intestinal oxalate secretion; (c) increased intestinal and circulating proinflammatory cytokines in obese subjects inhibits intestinal oxalate secretion mediated by the anion exchange transporter Slc26a6 (A6). The gene discussed is SLC26A6; the disease is obesity disorder.