It is notable that the cytokines IL-6, IL-1β, and TGFβ1 & β2 are transcriptional activators of hepcidin by the JAK/STAT and SMAD pathways [44,45], and the signal from cytokines supersedes the signal from Tf-iron [46–48], resulting in upregulation of hepcidin despite restricted availability of iron as in the anaemia of chronic inflammation. This evidence concerns the gene SOAT1 and anemia (phenotype).