This is an interesting phenomenon, and even though it could be due to an intrinsic characteristic of lymphocytes from RA patients, it is worth pointing out that one of the physiological functions of both ABCB1 and ABCG2 is cellular detoxification, including the active extrusion of inflammatory mediators such as TNF-α, IL-2, IL-12 and IFN-γ [24], and it is possible that the chronic exposure to increased levels of them could generate a greater transporter activity. The gene discussed is IFNG; the disease is rheumatoid arthritis.