Observation of higher hepcidin levels in children with SLE, and particular in children with lupus nephritis, may suggest not only that the use of hepcidin-antagonists could have a role in the treatment of the anemia of SLE in those with kidney disease, but also that such agents could interrupt the pathway for increased cardiovascular mortality in children with CKD and ESRD secondary to SLE. The gene discussed is HAMP; the disease is lupus nephritis.