The gastrointestinal tract expresses a multitude of Slc26 family members, several of them with ill-defined function. This presentation will focus on the three Slc26 isoforms that are highly expressed in the apical membrane of gastrointestinal epithelial cells, but with different segmental expression and, most importantly, different anion transport properties, as discussed by the first speaker. The Slc26a9 isoform is strongly expressed in the luminal membrane of the stomach, is also found in oesophagus and duodenum, the lung, and specialized cells of the kidney, pancreas, reproductive tract and neuronal system. Its genetic deletions results in a complete loss of gastric acid secretion and extensive fundic hyperplasia within a few weeks after birth. Duodenal HCO3- secretion is also altered in Slc26a9 knockout mice, particularly at young ages. Polymorphisms in this gene carry a higher risk of meconium ileus in cystic fibrosis newborns and a worse prognosis for CF diabetes. The Slc26a6 isoform is particularly strongly expressed in the upper small intestine, the renal proximal tubule, the pancreas, but at relatively lower levels in various other organs. Its genetic deletion results in reduced small intestinal HCO3- and oxalate secretion, the development of oxalate kidney stones in some mouse strains and small intestinal fluid and nutrient absorptive defects. A polymorphism in the Slc26a6 gene is associated with increased urinary oxalate excretion and hypertension. The Slc26a3 isoform is very highly expressed in the large intestine and the gallbladder and at lower levels in the small intestine, the pancreas and the reproductive system. Mutations in Slc26a3 are the molecular basis for congenital chloride-losing diarrhoea. These patients suffer from lifelong diarrhoea. One of the associated findings in long term follow up of larger patient cohorts is a high incidence of both acute and chronic intestinal inflammation. The Slc26a3-deficient mouse proved to be a good model for studying potential barrier defects in these mice that may explain the underlying pathophysiology, such as defective ion transport, an altered mucus barrier, and changes in the intestinal microbiome.