More importantly, higher YAP levels and lower E-cadherin levels were noted in the chronic gastritis tissues from H. pylori-positive patients compared to those from H. pylori-negative patients, suggesting that activation of the YAP signalling pathway at the stage of CNAG is one of the major molecular mechanisms H. pylori utilizes to promote the cascade of gastric carcinogenesis. The gene discussed is CDH1; the disease is chronic gastritis.