An increased level of fetal Hb in erythroid cells is observed in many divergent human conditions. Unlike the pancellular hereditary persistence of HbF syndromes, these conditions do not represent a failure of completion of the erythroid developmental program. but, rather, they are due to an alteration in the coordination of HbF and HbA expression in erythroid precursor cells. The erythropoietic stress associated with increased HbF production as seen in the pathologic conditions included in this study can also occur due to acute blood loss(16), marrow transplantation(17), erythroblastopenia of childhood(16), and severe iron deficiency(18). At a cellular level, studies suggest that this results from the selective recruitment of erythroid progenitors with the capacity to synthesize HbF. At a molecular level, the mechanisms responsible for this increase in fetal Hb synthesis remain unknown.