Gastric cancer develops in a stepwise manner along the inflammation–metaplasia–dysplasia–carcinoma pathway. Similar to several infection‐associated cancers, such as liver cancer (associated with viral hepatitis B and C) and cervical cancer (associated with human papilloma virus), Helicobacter pylori infection is the main trigger of this carcinogenic cascade. Observational studies with baseline serological testing and more than 10 years of follow up have found that chronic H. pylori infection is related to about 90% of gastric cancers and thus removal of this bacterium from a population has been postulated to eradicate the occurrence of gastric cancer.1 This hypothesis has stimulated numerous investigations indicating not only the magnitude of benefit obtained from a short‐course antibiotic treatment but also the principles to help policymakers design preventive services that maximize the effectiveness of using this strategy. The application of this antibiotic‐based approach for gastric cancer prevention has been hindered by a lack of answers to four important questions (Table ​(Table1).1). There are now satisfactory answers to these questions. Table 1 Questions about the elimination of gastric cancer through H. pylori eradication.