Aplastic anemia's long history, from its early description by Ehrlich (1) at the end of the 19th century, and the simplicity of its pathology, an empty bone marrow, have made it the paradigm of hematopoietic failure syndromes. Aplastic anemia is now increasingly recognized as being closely related to other hematologic diseases (Figure 1). Erythrocytes, granulocytes, and platelets, which are normally produced in the bone marrow, decrease to dangerously low levels. Blood cell counts determine presentation and prognosis. Anemia leads to fatigue, dyspnea, and cardiac symptoms; thrombocytopenia to bruising and mucosal bleeding; and neutropenia to sharply increased susceptibility to infection. When patients are treated with transfusions and antibiotics alone, survival rates are poor and related to the severity of the pancytopenia, as defined by the presence of two of three criteria: a neutrophil count less than 0.5 × 109 cells/L, a platelet count less than 20 × 109 cells/L, and a reticulocyte count less than 1%. When the neutrophil count is less than 0.2 × 109 cells/L, the disease is characterized as very severe. In the early 20th century, patients often died quickly of heart failure, profuse hemorrhage, or overwhelming infection. In the modern era of erythrocyte and platelet transfusions, the most common causes of death are recurrent bacterial sepsis or fungal invasion of critical organs secondary to refractory granulocytopenia.