In RA, a high level of 10.13039/501100007072IFN type I predicted the response to TNFα blockade, but not to rituximab, a B cell depleting monoclonal antibody, supporting the fact that 10.13039/501100007072IFN type I signature in RA induces a high inflammatory activity, but not an elevated autoantibody production by B cells based on the independence observed between 10.13039/100006600FLC levels and anti-10.13039/100005550CCP production [41]. This evidence concerns the gene TNF and rheumatoid arthritis.