Fetal erythropoiesis occurs during chronic bone marrow failure, or during recovery from marrow suppression. Fetal erythrocytes have HB F, with more G gamma than A gamma chains," i" antigen, large MCV, characteristic enzyme levels, low carbonic anhydrase, low HB A2, and short life span. Many of these fetal characteristics are present in the red cells of patients with temporary or chronic hematopoietic stress. In those in whom normal hematopoiesis ensues, the fetal erythrocytes disappear. The fetal phase of recovery may be with homologous stem cells after bone marrow engraftment, or with autologous cells. Chronic fetal erythropoiesis is seen in patients with constitutional aplastic anemia, such as Fanconi's anemia or Diamond-Blackfan anemia. In one patient with the latter disorder, fetal erythropoiesis accompanied chronic anemia, and actually decreased slightly during the acute phase of clinical improvement. Culture of late erythroid precursor cells (CFU-Es) from a patient with transient erythroblastopenia of childhood led to in vitro development of colonies with HB F, an event not seen in normal marrow cultures. Thus fetal erythropoiesis occurs during hematopoietic stress, whether chronic or transient, if there is some marrow activity, and may be due to expansion of fetal clones.