However, when CagA excess activates NF-κB and/or STAT3, it could induce the production of pro-inflammatory cytokines and anti-apoptotic proteins to promote the expansion of cancer-susceptible cells and prevent their apoptosis, which also induces ROS to increase DNA damage and accelerate the accumulation of mutations (Hatakeyama, 2014; Yong et al., 2015). Here, NFKB1 is linked to cancer.