Although it was originally described that TMPRSS6 is increased/stabilized by iron deficiency, erythropoietic drive or hypoxia, it has been shown that chronic iron overload and BMP6 levels can also induce TMPRSS6 expression, and such modulation could lead to a negative feedback mechanism to avoid an excessive stimulation of hepcidin induced by iron in order to maintain iron homeostasis [25]. The gene discussed is TMPRSS6; the disease is nutritional disorder.