The clearest clinical relationship is the well-demonstrated response of SpA to IL-17A inhibition therapy in contrast to a much less profound improvement in other types of inflammatory arthritis.42 43 Our finding that the Tc17 pathway is active in very early SpA may in part help explain these differences in response to IL-17 inhibition.44 Conversely, most arthritis types respond to inhibition of TNF,45 which was expressed at similar levels in all the arthritis types tested here. The gene discussed is IL17A; the disease is arthritic joint disease.