Sustained activation of the NF-κB signaling pathway leads to an elevated expression of inflammatory cytokines, such as TNF-α and IL-1β, which can promote the polarization of macrophages toward the M1 phenotype, increase damage to the extracellular matrix and degradation of the cartilage, and exacerbate RA ultimately [7,12]. This evidence concerns the gene NFKB1 and rheumatoid arthritis.