Additionally, a gene ontology and pathway analysis revealed increased expression of type I IFN-inducible genes in the peripheral blood of patients with RA.189 Higgs, B. W. et al. demonstrated that an overactive type I IFN pathway is involved in the disease activity of RA.190 Another study showed that miR-17 suppressed the secretion of proinflammatory cytokines such as IL-6 and IL-1β and bound to STAT3 and JAK1 to play an anti-inflammatory and anti-erosive role in RA development. This evidence concerns the gene IL1B and rheumatoid arthritis.