The difference in IFN values of RA and SSc patients compared to that of healthy individuals between the study [35] and ours might be due to their use of whole blood cells and different IIGs (IFI44, IFI44L, IFI27, RSAD2, and IFI6) that they had selected on the basis of increased IIGs among 5 diseases (SLE, RA, SSc, polymyositis, and dermatomyositis) [35], and those IIGs might be induced through the activation of the signaling pathways other than IFN pathways. This evidence concerns the gene RSAD2 and systemic sclerosis.