suppression benefits β-thalassemic erythropoiesis.

Abstract

Multiple studies in murine model systems of β-thalassemia have demonstrated that iron restriction improves the ineffective erythropoiesis characteristic of this disorder, the mechanisms of which have not yet been fully elucidated. In this issue of, Artuso et al demonstrate that erythroid knockout of transferrin receptor 2 () also improves hematologic parameters in β-thalassemic mice. The authors invoke changes in erythropoietin (Epo) sensitivity rather than erythroid iron delivery per se as the underlying mechanism.