The production of blood cells by the bone marrow depends on the availability of a sufficient number of functioning stem cells, which must be able to reproduce and renew themselves repeatedly to maintain a constant number, and to differentiate into granulocyte, red, and megakaryocyte systems, thereby continuously forming a large number of mature blood cells. Stem cell deficiency or defective function is the cause of reoccurrence. For example, bone marrow hematopoietic stem cell cultures from patients with severe reblasts show a decrease in directed progenitor cells, suggesting a decrease in pluripotent stem cells or dysfunction. Many patients with aplastic anemia have had successful bone marrow transplants. Suggesting that defects in the bone marrow can be corrected by implantation of normal bone marrow stem cells, stem cell deficiency or defects are the most common cause of this anemia. Pluripotent stem cells proliferate and renew under specific microenvironmental conditions. Aplastic anemia may also result from defects in the bone marrow hematopoietic microenvironment. Experiments have shown the importance of the bone marrow stroma or microenvironment in the proliferation and maturation of blood cells. If the stem cells do not grow in long-term culture unless an apposed cell layer is obtained from normal bone marrow, they will not grow. Successful bone marrow transplantation does not exclude microenvironmental abnormalities, as stem cells from the microenvironment are transplantable, and defects in the bone marrow microenvironment lead to insufficient stem cell function resulting in allogeneic cytopenia, which is the minority of cases. Bone marrow stromal cells can produce hematopoietic growth factors, such as GM-CSF, which are supplied to the progenitor cells. However, the factors regulating hematopoiesis, such as colony-stimulating factor and erythropoietin in blood and urine, increase during reoccurrence, so the occurrence of reoccurrence may not be due to a decrease in these factors. It may also be the result of suppression of hematopoietic cells by cellular or humoral immunity. In recent years attention has focused on immunosuppression of hematopoietic cells. As in the case of successful treatment of reblasts with anti-lymphocyte serum, immunosuppressive therapy is often required in identical twin transplants, where only 50% of patients with identical twin reblasts have successful bone marrow transplants and the remaining 50% can only succeed with immunosuppression for pretreatment. Suppressive T lymphocytes have been shown to inhibit the growth and differentiation of stem cells. Aplasia may also be caused by anti-stem cell antibodies or anti-cellular antibodies against hematopoietic precursors. The pathogenesis hypothesis of aplastic anemia has been compared to the relationship between pluripotent stem cells, the hematopoietic microenvironment and the immune response as “seed” (seed), “soil” (soil) and “worm” (worm). The relationship between “seed” (seed), “soil” (soil) and “worm” (worm), and possibly “fertilizer” (fertilizer) has been likened to the relationship between these components, of which defects in any of them may lead to the onset of reperfusion.