In addition, exposure to pathogenic antigens such as LPS could induce TLR4 signaling pathway which subsequently induces NF-κB activation and expression of pro-inflammatory cytokines such as TNF-α, and IL-1β, IL-6, resulting in an imbalance between pro-inflammatory and anti-inflammatory cytokine activity and contributes to the pathogenesis of RA (Fu et al., 2013; Zhu et al., 2016). This evidence concerns the gene IL1B and rheumatoid arthritis.