In the pathogenicity of rheumatoid arthritis, ROS, which are considered to be enhancers of inflammatory proliferation of the synovial membrane, play a key role in that their increased production increases the destruction of cartilage and even bones, activates or removes NF-κB transcription factor, induces the production of many cytokines, and activates enzymes such as COX and 5-lipoxygenase or even inducible nitrogen monoxide [62–65]. Here, NFKB1 is linked to rheumatoid arthritis.