GAST and chronic atrophic gastritis: This creates an ulcer-prone environment in which the pH neutralization processes in the duodenum are overwhelmed.77 In contrast, non-ulcer patients presenting with corpus-dominant or pangastritis exhibit reduced oxyntic sensitivity to gastrin (2-fold reduction), likely as a result of widespread inflammation in the gastric body.78 As a consequence, H. pylori infection results in achlorhydria and promotes atrophic gastritis, bacterial overgrowth, and gastric metaplasia, a microenvironment predisposing to gastric cancer.79–81