Preclinical studies in mouse models of iron overload have shown that long acting hepcidin analogs, also referred to as minihepcidins [135,136], and antisense oligonucleotides targeting TMPRSS6, a metalloprotease that inhibits endogenous hepcidin production [137], effectively decrease iron load, improve erythropoiesis, and increase hemoglobin concentrations, thus showing merit for further clinical investigation. The gene discussed is TMPRSS6; the disease is Tangier disease.