Based on these findings it has been proposed that the ferroxidase activity of APP in Alzheimer’s disease has the same function as the ferroxidase activity of ceruloplasmin coupled to iron-export activity of ferroportin [14]: the Fe(II) ion that is exiting ferroportin binds to the ferroxidase site of APP, it is oxidized by molecular oxygen, and the resulting Fe(III) product is then scavenged by the ferric binding protein, transferrin. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.