Macrophages, the immune cells against invading pathogens, have a cardinal role in innate immune response.1, 2 However, excessively activated macrophages usually cause the aberrant release of inflammatory mediators involved in diversified inflammatory diseases, such as rheumatoid arthritis, sepsis, and inflammatory bowel disease.3, 4, 5 Thus the inhibition of inflammatory mediators such as TNF-α, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1β, and IL-6 is the priority in the development of new anti-inflammatory drugs. The gene discussed is PTGS2; the disease is rheumatoid arthritis.