It should be noted that in malignancies induced (or accompanied) by constant damage and chronic inflammation like HCC, two factors can further impinge on iron trafficking: on the one hand, TAM are more M1-like (107) and could restrict iron availability in the microenvironment and exert toxicity against malignant cells; on the other hand, the high hepcidin levels caused by inflammation may weaken Fpn-mediated iron release from macrophages, thus contrasting the iron-donating activity of TAM. This evidence concerns the gene SLC40A1 and hepatocellular carcinoma.