Yi’s review indicates that CK, G-Rb1, Pn-BE, and PNS ameliorate RA by decreasing MMP-1, MMP-9, MMP-13, TNF-α, IL-1β, iNOS, and NF-kB/MAPK signaling, clinical arthritis scores, cartilage destruction, immune cell infiltration, and onset/progression of RA and by improving arthritis clinical symptoms in various cells, animal models, and human RA patients [48]. The gene discussed is NFKB1; the disease is arthritic joint disease.