Notably, a correlation between the upregulation of CEACAM1 and the activation of the non-canonical NF-κB pathway in H. pylori-induced gastritis, intestinal-type, and diffuse-type gastric tumors was also reported (22), strongly indicating a vital contribution of CEACAM1 to the pathogenic hallmarks of H. pylori infection. This evidence concerns the gene CEACAM1 and gastritis.