Down the repressors! Up the fetal hemoglobin!

Abstract

One of the major goals of hemoglobinopathy research has been to devise improved pharmacologic strategies for the induction of fetal hemoglobin (HbF) in people with sickle cell disease and β-thalassemia. In this issue of Blood, Dulmovits and colleagues report that pomalidomide, a drug approved by the US Food and Drug Administration (FDA) for treatment of multiple myeloma, induces HbF production by decreasing levels of several key transcriptional repressors of fetal globin gene expression.1 In addition, they show that pomalidomide induces HbF in differentiating erythroid cells from people with sickle cell disease and in myeloma patients.