Such an association was in line with previous findings, demonstrating that patients with a low IFN signature had a significantly greater reduction of disease activity and more often achieved a significant response.92 Clinical utility as predictor of non-response to rituximab was demonstrated in a validation study using ROC curve analysis, based on an optimal set of 3–5 IFN type I genes according to the differential disease activity score.91 These results suggest that RA patients with an IFNhigh signature represent a different pathogenic subset of patients. The gene discussed is IFNA1; the disease is rheumatoid arthritis.