Because COX-2-derived TxA2 is not the molecular target of NSAIDs and DMARDs, the limitations and negative side effects of those drugs may be, at least in part, attributable to lack of the effects on the COX-2/TxA2 pathway, which coupled with the positive role of the COX-2/TxA2 pathway in pathogenesis of RA suggests that the pharmacological approaches targeting this pathway hold the potential as a novel add-on therapy in therapeutic strategy of RA (Figure 3). The gene discussed is PTGS2; the disease is rheumatoid arthritis.