Because the salivary glands of SS patients contain T cells that express IFNγ and Stat1 mRNA [24], with these T cells being predominantly Th1 cells [25], the proinflammatory cytokine IFNγ has been considered a principle mediator of inflammation in SS patients, similar to TNFα in patients with RA [3]. The gene discussed is STAT1; the disease is rheumatoid arthritis.