Growing evidence show that the pathogenesis of RA may be related to the defects in immune-modulation and a host of inflammatory mechanisms [20–22], thus, the differentially expressed genes, such as CRK, GHR, RNF2, RNF8, VAV2, which are involved into these biological processes might influence the therapeutic effects of TG tablets in controlling inflammation response and regulating immunity during RA progression. Here, RNF2 is linked to rheumatoid arthritis.