NFKB1 and gastric cancer: In addition, H. pylori activates multiple intracellular pathways in epithelial cells, such as the NF-κB, β-catenin pathway and PI3K/AKT pathway, which induces increased inflammatory cytokine production, altered apoptosis rate, and deregulated epithelial cell proliferation and differentiation, finally leading to the oncogenic transformation of early human gastric cancer (78, 82–88).