Gastric cancer (GC) develops through a multistep process known as the gastritis-atrophy-metaplasia-dysplasia-cancer sequence associated with alterations in the expression of host oncogenes and tumor suppressor genes after several decades. Helicobacter pylori (H. pylori) infection is the most consistent risk factor for GC, and its elimination is, therefore, the most promising strategy to reduce the incidence of this malignant disorder. However, the results of the relevant studies are controversial as to whether the H. Pylori eradication effectively induces the regression of gastric preneoplastic lesions. The inconsistencies are likely due to the heterogeneity in studies with respect to the number of biopsy samples taken, the method of histologic classification of findings, sample size, and the duration of the follow-up. Additionally some probable or well-defined factors other than H. Pylori may influence the progression of gastric preneoplastic lesions. Lastly, the real existence of a point of no return may partially explain the controversial findings. Here, we present an index case, and review data about the role of H. pylori during gastric carcinogenesis, and subsequently discuss information available from recent studies to evaluate the benefit of the H. pylori eradication for the regression of gastric precancerous lesions.