As non-transferrin-bound iron may trigger oxidative damage and an inflammatory response [34, 35], we speculate that increasing transferrin and sTfR concentrations would probably prevent dyslipidaemia and lipid deposition, the early stage of atherosclerosis, by acting as iron-binding proteins and thus reducing labile iron and the subsequent production of very damaging oxidative radicals. The gene discussed is TF; the disease is atherosclerosis.