In such cases, a conserved motif in the C-terminal region of CagA known as the conserved repeat responsible for phosphorylation-independent activity (CRPIA) motif may interact with activated MET, leading to the activation of PI3K/Akt signaling for the proliferation of gastric cancer cells after H. pylori infection, which in turn contributes to the H. pylori-associated chronic gastric proliferative reaction and NF-kB signaling associated with the pro-inflammatory responses [48]. This evidence concerns the gene NFKB1 and gastric cancer.