Several studies have demonstrated that CagA-positive H. pylori infection induces abnormal Hippo signaling in GECs and promotes the activation and nucleation of the critical effector molecule YAP, during which CagA upregulates LATS2 and significantly increases the expression of YAP and TAZ, which induces the expression of downstream target genes, thereby inducing EMT and intestinal epithelial to increase the risk of early GC (Figure 2E) (Mo et al., 2015; Molina-Castro et al., 2020). The gene discussed is S100A8; the disease is gastric cancer.