In our research group, it has been proposed that the differential response to rhMIF between CS and RA could be mediated by a higher expression of MIF receptors in the PBMC of patients, since it has been reported that RA patients have high CXCR4 expression levels in synovial tissue CD4(+) memory T cells [27] and, therefore, something similar could be happening with the other MIF receptors. The gene discussed is CD4; the disease is rheumatoid arthritis.