In contrast to other inflammatory diseases, which are characterized by a hyperferritinemia with elevated hepcidin but without an iron overload (reduced transferrin saturation and SI), e.g. as in lupus erythematosus and rheumatoid arthritis [33–35], the hyperferritinemia in AIH-1 with subsequent BR appears to be deregulated from hepcidin. This evidence concerns the gene HAMP and lupus erythematosus.