The article discusses the role of *Helicobacter pylori* in gastric cancer and other related diseases. *H. pylori* is the dominant species in the human gastric microbiome and its infection causes persistent gastritis, which is the strongest risk factor for stomach cancer. However, only a small proportion of infected individuals develop malignancy, and the carcinogenic risk is influenced by bacterial components, host responses, and specific host-microbe interactions. The article highlights the importance of understanding these interactions for developing prevention strategies and gaining insights into inflammatory carcinomas beyond the stomach. Key bacterial components, such as the vacuolating cytotoxin (VacA) and the cag pathogenicity island, are discussed in detail, along with their mechanisms of action and their impact on host cell signaling pathways. The article also explores the reciprocal relationships between *H. pylori* and other diseases, such as oesophageal and allergic diseases, and the role of β-catenin in gastric carcinogenesis. Finally, it emphasizes the broader implications of these findings for understanding and treating various cancers arising from inflammatory foci in the gastrointestinal tract.The article discusses the role of *Helicobacter pylori* in gastric cancer and other related diseases. *H. pylori* is the dominant species in the human gastric microbiome and its infection causes persistent gastritis, which is the strongest risk factor for stomach cancer. However, only a small proportion of infected individuals develop malignancy, and the carcinogenic risk is influenced by bacterial components, host responses, and specific host-microbe interactions. The article highlights the importance of understanding these interactions for developing prevention strategies and gaining insights into inflammatory carcinomas beyond the stomach. Key bacterial components, such as the vacuolating cytotoxin (VacA) and the cag pathogenicity island, are discussed in detail, along with their mechanisms of action and their impact on host cell signaling pathways. The article also explores the reciprocal relationships between *H. pylori* and other diseases, such as oesophageal and allergic diseases, and the role of β-catenin in gastric carcinogenesis. Finally, it emphasizes the broader implications of these findings for understanding and treating various cancers arising from inflammatory foci in the gastrointestinal tract.