SLC40A1 and metabolic dysfunction-associated steatotic liver disease: Increased iron accumulation in liver in NAFLD might be due to the decrease in levels of the iron export protein ferroportin induced by the decrease of the iron regulatory peptide hepcidin [14]: liver synthesis of hepcidin is up-regulated in response to increased iron stores and inflammation; hepcidin enhances the degradation of ferroportin which allows Fe release [17,45,46]; increased expression of hepcidin and lower expression of ferroportin in patients with NAFLD could result in iron retention [46].