The differences between the effects of TNF blockade on IFN response activity between the studies in SS [11] and SoJIA [9], on the one hand, and our studies in RA and spondyloarthritis (SpA) [31], on the other, could have their origin in differences in design between the studies, such as the use of infliximab in RA versus etanercept in SS, and the different readout systems used. The gene discussed is TNF; the disease is rheumatoid arthritis.