It is generally believed that the pathogenesis of RA is related to genetic, infectious, and sex hormone factors, but it has also been shown that cytokines play a fundamental role in causing RA-related inflammation, joint destruction, and extra-articular manifestations (Brennan and McInnes, 2008), and RA synovitis is characterized by inflammatory infiltration and a synovial environment dominated by pro-inflammatory cytokines and chemokines (McInnes and Schett, 2007), in which IL-23, as a pro-inflammatory cytokine, is involved. The gene discussed is PLXNA3; the disease is rheumatoid arthritis.