Contrarily, it had highly significant positive correlation with hemoglobin.<h4>Conclusions</h4>High level of GDF15 and/or ERFE may inhibit hepcidin production and increase iron load in patients with thalassemia; therefore, medications that suppress their actions may provide new therapeutic potentials for iron toxicity.<h4>Impact</h4>Iron overload continues to be a major contributor to high morbidity and mortality in patients with thalassemia. This evidence concerns the gene GDF15 and thalassemia.