The relationship between Helicobacter pylori (H. pylori) and humans remains a complex enigma. While other factors contribute to gastric cancer (GC), their impact pales in comparison to the central role of H. pylori. Various cofactors, such as dietary carcinogens and Epstein-Barr virus infection, can lead to GC independently of H. pylori. However, it is likely the combination of mechanisms, especially those driven by H. pylori, that represents the primary force behind GC development. Identifying individuals at high risk of developing H. pylori-related GC or detecting the disease in its earliest stages remains a significant challenge. To address this, we aim to refine the existing gastric carcinogenic model by incorporating molecular data, oncological concepts common to many cancers, and data from innovative experimental approaches. This updated model, applicable to both intestinal and diffuse GC, builds on Pelayo Correa's carcinogenesis pathway while expanding our understanding of H. pylori's role in gastric carcinogenesis. It not only emphasizes the direct cellular effects of H. pylori virulence factors but also integrates underrecognized carcinogenic mechanisms, including the interactions between H. pylori and stem cells, providing a more comprehensive view of H. pylori's contribution. By acknowledging additional molecular drivers in GC and recognizing H. pylori's potential involvement in these processes, this model could offer more precise interpretations of GC development and open new avenues for clinical interventions.