The proposed mechanism for the progression of GC induced by TLR4 expression in GC cells is as follows: activated TLR4 signaling induces the formation of more ROS, especially mROS, and the resulting oxidative stress contributes to the upregulation of phosphorylated Akt, NF-κB p65 activation and nuclear translocation, which leads to GC cell proliferation. The gene discussed is NFKB1; the disease is gastric cancer.