However, both iron chelation and blockade of transferrin receptor-mediated iron uptake have been shown to stimulate EPO production, suggesting that iron deficiency itself may increase EPO levels.[27] There is also evidence that iron is required for degradation of HIF, suggesting that iron deficiency can increase levels of HIF and EPO levels.[28, 29] Data regarding the use of iron supplementation, which can decrease EPO levels, was not available at time of sampling.[30]. The gene discussed is TFRC; the disease is nutritional disorder.