Third, while the effects of both the principal STAT1-activating cytokine IFN-γ and STAT6-activating IL-4 seem either advantageous or disadvantageous depending on the phase of the arthritic disease or the animal model used [24,27,28], activation of STAT1 and STAT6 in response to these cytokines with respect to the RA progression and treatment response remain largely unknown. The gene discussed is IL4; the disease is rheumatoid arthritis.