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This review integrates the new thinking about relationships between gastric cancer and intestinal metaplasia/pseudopyloric metaplasia (SPEM). We address whether recent studies have closed or widened the knowledge gap regarding gastric cancer pathogenesis in mice or humans.Recent studies in mouse models have provided a variety of new insights into the cellular origin and progression of events resulting in gastric cancer. Many suggest a direct transformation from intestinal metaplasia/pseudopyloric metaplasia/SPEM to gastric cancer. However, results from different investigator and models are conflicting and often describe events not present in studies in humans.Both Helicobacter pylori-associated and autoimmune gastritis may produce gastric atrophy with extensive intestinal metaplasia and an abnormal gastric microbiome. However, only H. pylori gastritis carries a risk for adenocarcinoma. The differences reported with mouse models can best be explained as the results of different models of regeneration and repair rather than as models of gastric cancer. Overall, the data remains consistent with the original hypothesis that gastric cancer results from increased genetic instability of gastric stem cells rather than a direct transition from metaplasia to cancer. Intestinal metaplasia, pseudopyloric metaplasia, and SPEM have all been falsely accused based on guilt by association.