In spite of the repressing effect of ESAs and erythropoiesis products on hepcidin, its level is still very high in ESRD patients on dialysis (twofold the control values), reducing iron absorption and mobilization from iron stores; we can hypothesize that when ferritin reaches a certain threshold, increasing even more hepcidin synthesis, it will allow worsening of anemia, of iron disturbances, and hyporesponse to ESA therapy. The gene discussed is HAMP; the disease is anemia (phenotype).