By 14 months of age, all of the Slc26a9-deficient mice (23/23) exhibited a severe gastric preneoplastic phenotype, including chronic atrophic gastritis (CAG), mucous cell metaplasia, profound cyst formation and high-grade intraepithelial neoplasia (HGIN), equivalent to early GC [10, 12] (Fig. 1, c). Here, SLC26A9 is linked to gastritis.