We explored the mechanism of iron-induced heart disease at an early stage of acquired iron-overload in WT mice which displayed clear evidence of iron injury as reflected by myocardial accumulation of iron (Fig. 2A) and the increased and decreased expression of iron metabolic genes, ferritin L/H and ferroportin, and transferrin receptor 1 (Trfc1), respectively (Fig. 2B). This evidence concerns the gene SLC40A1 and heart disorder.