Yang et al. found that the anti-rheumatoid arthritis (RA) drug Auranofin at a normal dose (5 mg/kg) could up-regulate the expression of hepcidin-coding gene hepcidin antimicrobial peptide (HAMP) gene through the NF-kB/IL-6/STAT3 signaling pathway, reducing the intracellular iron load and the sensitivity of cells to ferroptosis (Yang et al., 2020), indicating that hepcidin can be utilized as a new strategy for regulating ferroptosis. The gene discussed is NFKB1; the disease is rheumatoid arthritis.