In the present invention, inventor identified the hepatokine FGL1 as a previously undescribed suppressor of hepcidin that is highly induced in the liver in response to hypoxia during the recovery from anemia and in thalassemic mice. They demonstrated that FGL1 is a potent suppressor of hepcidin in vitro and in vivo. Deletion of Fgl1 in mice (Fgl1 -/-) results in a lower repression of hepcidin after bleeding. Finally, inventors clearly demonstrate the FGL1 is a BMP antagonist that directly binds BMP6 to impair the canonical BMP-SMAD signaling cascade that governs hepcidin regulation. So, the present invention relates to a method for preventing or treating iron overload associated diseases by targeting the new hepcidin repressor, the hepatokine FGL1.