Apart from a potential specific function of the deleted Slc26a9 gene for gastric epithelial function, the loss of parietal cells and the ensuing hypo/achlorhydria that are uniformly present in many mouse models of oxyntic atrophy/metaplasia and neoplasia, will initiate a cascade of events that are conducive to neoplasia development. The gene discussed is SLC26A9; the disease is neoplasm.