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Gastric cancer is a major global health concern, with ongoing efforts focused on screening and eradicating Helicobacter pylori infection.1 However, H. pylori infection is typically acquired during childhood, and gastric cancer develops through a multistage process of carcinogenesis, progressing from chronic active gastritis to atrophic gastritis, then to intestinal metaplasia, and ultimately to gastric cancer. Irreversible damage may occur along this long pathway, and eradicating H. pylori may not completely eliminate the risk of gastric cancer. Effective methods for properly integrating primary prevention with secondary prevention through upper endoscopic screening are warranted, but reliable and accurate biomarkers for endoscopy remain an unmet need. Although direct endoscopic examination, including the image-enhanced approaches and histological assessments of seemingly normal gastric mucosa, may provide a solution, evaluating the extent and severity of premalignant conditions is labour-intensive, subject to inter-rater variability and complicated by the uncertainty regarding the optimal number and location of endoscopic biopsies.2 Given the typically patchy distribution of premalignant lesions, even a standardised endoscopic biopsy protocol may have limited predictive value, as it relies on a small number of biopsy samples.