Ineffective erythropoiesis is the hallmark of beta-thalassemia that triggers a cascade of
compensatory mechanisms resulting in clinical sequelae such as erythroid marrow
expansion, extramedullary hematopoiesis, splenomegaly, and increased gastrointestinal
iron absorption. Recent studies have begun to shed light on the complex molecular
mechanisms underlying ineffective erythropoiesis and the associated compensatory
pathways; this new understanding may lead to the development of novel therapies …