These data include the association between high expression MIF alleles and renal injury (7), the ameliorative effect of immunoneutralization or genetic deletion of MIF on experimental lupus nephritis (12, 13), and the overexpression of the MIF receptor CD74 in glomerulonephritis (26), all observations that have contributed to the scientific rationale for the ongoing clinical evaluation of a humanized anti-MIF receptor (anti-CD74) (27). This evidence concerns the gene MIF and glomerulonephritis.