Several other factors can induce HIF-1α via regulating reactive oxygen species (ROS) or kinases, and gastric epithelial ROS, whether endogenous or induced by H. pylori, enhance HIF-1α expression in gastric mucosa under normoxic conditions.10 Importantly, HIFs have emerged as major transcriptional regulators of immunity11 and are involved in cancer progression.12,13 Thus, we sought to investigate the role of HIF-1α in the development of gastric inflammation and injury within the context of H. pylori infection. This evidence concerns the gene HIF1A and cancer.