Taken together with previous reports of SLC26A9-associated pancreatic phenotypes [13–15] we purport that SLC26A9 may provide alternative chloride transport at early developmental stages, and that its contribution to meconium ileus, is at least partly, from the pancreas. This evidence concerns the gene SLC26A9 and intestinal obstruction in the newborn due to guanylate cyclase 2C deficiency.