It seemed that TRIP could interact with TAK1 and promote TAK1 K48-linked polyubiquitination and degradation without stimuli added, it may be caused by the self-production of TNFα or other cytokines of RA-FLS, and the weak interaction between TRIP and TAK1 may be due to the low level of these cytokines of unstimulated RA-FLS. This evidence concerns the gene TRAIP and rheumatoid arthritis.