This observation is very intriguing because it connects the iron-mediated regulation of GDF15 concentration to patho-physiological levels of iron: despite systemic iron overload, ineffective erythropoiesis and associated iron-fluxes in beta-thalassemia might generate an iron deficiency signal in a relevant molecular or cellular context and consequent stimulation of GDF15 expression in a particular erythroid compartment [93]. Here, GDF15 is linked to nutritional disorder.