Given that the human gastric pathogen H. pylori exerts much of its pathogenicity by inducing DNA damage and apoptosis in host gastric epithelial cells [33], BCL2L11, CASP7, and CD79B reported to be linked to apoptosis [34]–[38] and RAD50 and ACAA1 reported to be linked to the DNA damage and repair system in relation to gastric cancer development [39], [40] also showed a biological plausibility. This evidence concerns the gene CD79B and gastric cancer.