The positive correlation between the SF TXN and the serum C Reactive Protein in the absence of a high concentration of SF TNF-α may indicate that TXN is involved in the prolongation and persistence of the RA inflammation, because high concentrations of TXN could stimulate NF-kB activation in the presence of the otherwise insufficient concentration of TNF-α [52]. This evidence concerns the gene CRP and rheumatoid arthritis.