Several intracellular signaling molecules are reportedly involved in the pathogenesis of RA (e.g., PDGFR, nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), SYK, and Bruton’s tyrosine kinase (BTK)), and inhibition of these molecules could prove beneficial for patients with RA [3, 13]. Here, NFKB1 is linked to rheumatoid arthritis.