Critically, iron homeostasis is disrupted during GVHD, where donor T cell-mediated injury to the intestinal mucosa and liver impairs hepcidin regulation, a key hormone encoded by the Hepcidin Antimicrobial Peptide (HAMP) gene, leading to uncontrolled ferroportin-mediated iron export and systemic iron accumulation [3,4]. The gene discussed is HAMP; the disease is graft versus host disease.