ESR1 and chronic atrophic gastritis: Previous data have demonstrated that gastric epithelial cells express the estrogen receptor, and hence a direct abrogation of signaling through this receptor is a biologically plausible mechanism for inducing gastric atrophy; however, the similarity of lesions induced in the stomach following tamoxifen with that induced by known protonophores including DMP-777 has also promoted the concept of tamoxifen acting as a direct epithelial cell toxin.10 Our DNA damage assays suggest that genotoxic stress may contribute to the gastric lesions induced by tamoxifen.