It is well known that MIF acts via CD74 to exert its biological activities in many kidney diseases,44 and that deletion of CD74 can protect against NTS‐induced acute kidney disease.45 Thus, in the present study, genetic deletion of MIF led to the down‐regulation of CD74 and TLR4 and consequently to the inactivation of downstream NF‐κB signalling and the inhibition of NF‐κB‐dependent renal inflammation. This evidence concerns the gene CD74 and kidney disorder.