Abstract: Helicobacter pylori (Hp) is currently classified as a class I carcinogen that can cause gastric cancer, research in recent years on how Hp infection causes the occurrence and progression of gastric cancer has attracted much attention. As the primary virulence factor of Hp, cytotoxicity-associated gene A (CagA) has been extensively studied and reported to function as a key excreted toxin for Hp to induce gastric infection, colonization and promote inflammatory-carcinogenic transformation of host cells. Patients infected with CagA-positive strains have a higher risk of developing tumors compared to those infected with CagA-negative strains. Based on previous studies, this article further elaborates on the import process, biological activity, and related molecular mechanisms of virulence protein CagA in the occurrence and development of gastric cancer induced by Hp infection.