The efflux of iron is primarily mediated by the ferroportin (FPN, encoded by the SLC40A1 gene) – hepcidin (encoded by the Hepcidin Antimicrobial Peptide (HAMP) gene) axis, among which hepcidin is a cysteine‐rich antibacterial polypeptide capable of binding to FPN and facilitating its degradation.[3, 44] One study indicated that in macrophages, the oxidative stress triggered by short‐term copper loading activated NRF2 and then facilitated the expression of FPN.[45] However, the regulatory effect of copper on FPN in tumor cells has not been verified. The gene discussed is HAMP; the disease is neoplasm.