Differences in extent of parietal cell atrophy and impact on gastric pH probably contribute to the divergence in clinical manifestations, driving prominent ECL cell hyperplasia and neuroendocrine tumor development in AIG but not Hp. AIG initiates and remains restricted to the corpus of the stomach primarily targeting parietal cells, whereas Hp initially colonizes the antrum and spreads through to the corpus after long-standing infection, causing a patchy or multifocal disease (Graham et al., 2019). This evidence concerns the gene HP and neuroendocrine neoplasm.