I F the bone marrow possessed an unlimited capacity for erythropoiesis, no anemia would develop in hemolytic disease. As fast as red cells were destroyed they would be replaced. Even without such an ability the marrow, as it actually exists, can compensate for a considerable amount of abnormal blood destruction. Anemia results only when the hemolytic process overtaxes the regenerative capacity. The limit of the human bone marrow’s ability to produce red cells in response to increased demand has never been established. In chronic hemolytic disease, as exemplified by the hereditary hemolytic anemias, the regenerative effort of the bone marrow appears to be rather constant. Unless some sort of crisis intervenes the hemoglobin level of such patients, with or without anemia, tends to remain fairly static month after month. Hemolysis and erythropoiesis are in equilibrium, even as they are in normal people, but the rate of exchange is faster than normal. The existence of anemia in a patient with chronic, stabilized hemolytic disease suggests that his bone marrow is working at or very near its capacity but despite the effort is unable to produce enough hemoglobin to maintain a normal level in the circulation. In order to ascertain the limits of hemoglobin and red cell synthesis during the sustained heav) demand of such a disease, we have examined the problem in two patients with hereditary hemolytic anemia. acute respiratory infection and the presence of splenomegaly drew attention to his underlying disease. The diagnosis was confirmed by a family study. The anemia was later cured by splenectomy. The second patient, together with his family, has been the subject of a previous report.3 Although the hemolytic anemia was hereditary, it was different from hereditary spherocytosis for there were no spherocytes, and splenectomy proved to be of no value. The disease was also different from other known forms of hereditary and familial anemia. The patient was originally admitted to the hospital with an acute arthritis which had subsided long before the present study was begun. The bone marrow of both patients, aspirated on several occasions from various sites, showed marked erythroid hyperplasia. Over a period of observation of many consecutive months, the degree of anemia and jaundice of these patients was found to be quite constant. The hematocrit did not vary * 2 from the values shown in Table I. The plasma bilirubin ranged between 1.8 and 4.0 mg. per 100 cc. Thus both patients had a chronic, moderate, well stabilized hemolytic anemia with generalized hyperplasia and hyperactivity of the bone marrow. Both were healthy except for the blood dyscrasia and both were well nourished on a good hospital diet.