It has been demonstrated that an orally bioavailable MIF antagonist, (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) [33], inhibited the interaction between MIF and CD74 and reduced functional and histological indices of glomerulonephritis, CD74(+) and CXCR4(+) leukocyte recruitment, and proinflammatory cytokine and chemokine expression in the NZB/NZW F1 and the MRL/lpr mouse strains, two distinct models of SLE [34]. This evidence concerns the gene MIF and glomerulonephritis.