These results raise the question of whether the expression of Slc26a9 is reduced during Helicobacter pylori (H. pylori, Hp) infection due to the production of ammonia (NH3)/NH4+ through its urease activity, which may predispose patients to acidic injury and peptic ulcers by impairing Slc26a9-mediated gastric HCO3- secretion. This evidence concerns the gene SLC26A9 and Peptic ulcer.