Research suggests that the Helicobacter pylori VacA toxin causes cell death, with possible mechanisms including the accumulation of cytoplasmic connexin 43, engagement of the mitochondrial fission machinery, and induction of autophagic cell death via the endoplasmic reticulum stress pathway. The toxin's effects on host cells may also involve disruption of cellular mechanisms, including mitochondrial function and metabolism. The relationship between Helicobacter pylori VacA and cell death is being studied in the context of gastric cancer and other infections.