Current research has shown that a variety of virulence factors produced by H. pylori, for instance, CagA, VacA, HtrA, Baba, Saba, and oipa, can help it attach to gastric epithelial cells, cause the host immune system to release various pro-inflammatory cytokines and chemokines and activate multiple signal pathways, such as the NF-κB, Wnt/β-catenin, and PI3K/Akt/mTOR pathways, which affect cell proliferation and differentiation, and promote the transformation of normal gastric epithelial cells into cancer cells [50, 51]. This evidence concerns the gene NFKB1 and cancer.