**1. Introduction**

The Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) signaling pathway play a fundamental role in regulating chronic systemic inflammatory responses in rheumatoid arthritis (RA) [1-5], based on compelling evidence that JAK/STAT is activated by many of the pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-2, IL-3, IL-6, IL-12, IL-17, IL-18, IL-19/IL-20, interferon-α/γ (IFN-α/γ) and oncostatin M (OSM) which are well-known to regulate, in part, immune-mediated inflammation in several autoimmune diseases, including RA [6-10]. However, complicating matters is the fact that some of the an‐ ti-inflammatory cytokines, which are known to dampen inflammatory responses induced by pro-inflammatory cytokines, including, IL-4, IL-10 and IL-13 also activate JAK/STAT [11-14]. In this regard, Müller-Ladner *et al*. [15] showed that synovial tissue obtained from RA pa‐ tients contained significant amounts of constitutively activated IL-4/STAT. Therefore it will be necessary to understand more precisely the extent to which pro- and/or anti-inflammato‐ ry cytokine gene expression is deregulated in RA and which of the STAT-responsive genes known to alter immune-mediated inflammation in response to these cytokines may be ame‐ nable to therapeutic intervention.
