The impact of the cytokine environment in the blood may co-determine the stimulation outcome in RA prior to treatment compared with the control, whereby the decrease in inflammation due to the effect of TNFi treatment reduced the levels of TNF and other inflammatory cytokines that could account for the decreased levels of p38, NF-kB and Erk1/2 phosphorylation after TNFi treatment in the RA patient. This evidence concerns the gene NFKB1 and rheumatoid arthritis.