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Two placebo-controlled trials reported in this issue of the Journal show the efficacy of an oral Janus kinase (JAK) inhibitor, tofacitinib, in the treatment of rheumatoid arthritis.1,2 If this agent is approved by the Food and Drug Administration (FDA) for use in patients with rheumatoid arthritis, clinicians will confront several complex questions. What is the rationale for targeting this family of kinases? How effective is tofacitinib as compared with other proven agents that are used to treat rheumatoid arthritis? What safety concerns need to be kept in focus? How should JAK inhibition be combined with other medications in the . . .
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David A. Fox (2012) studied this question.
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