PRF1 and chronic atrophic gastritis: The major gastric autoantigen is H+/K+-ATPase, and gastric T-cell recognition of H+/K+-ATPase results in secretion of Th1 cytokines and activation of perforin- and FasLigand-mediated cytotoxic killing of parietal cells, leading to gastric atrophy, a preneoplastic lesion of gastric cancer (12, 24, 25).