Extracellular vesicles (EVs) are cell-derived vesicles that play a critical role in host-pathogen interactions, facilitating intercellular communication and transporting both pathogen- and host-derived molecules during infection spread. To regulate their environment, for instance, by modulating innate and adaptive inflammatory immune responses, pathogens may alter the composition of EVs produced by infected cells. Gastric cancer is one of the leading causes of cancer-related deaths worldwide, and Helicobacter pylori infection is considered a significant risk factor for its development. This cancer is characterized by significant inflammation mediated by EVs generated from infected host cells. H. pylori contributes substantially to inflammation, promoting disease progression. Moreover, H. pylori produces and releases vesicles known as outer membrane vesicles (H. pylori-OMVs), which contribute to the shrinkage and cellular transformation of the gastric epithelium. Although the vacuolating cytotoxin A (VacA) plays a critical role in pathogenesis, its association with EVs in H. pylori has not been previously addressed. Understanding the roles of extracellular vesicles and VacA during H. pylori infection-whether they benefit the host or the pathogen-could pave the way for new treatment approaches. This review briefly discusses the role of VacA and extracellular vesicles in the growth and pathogenesis of