Erythropoietin (EPO) is a glycoprotein hormone that stimulates the production of erythrocytes in red bone marrow. Although EPO is primarily produced and released by the kidneys in response to low tissue levels of oxygen, several other tissues, including the liver and neurons of the central nervous system (CNS), can produce EPO. EPO binds the EPO receptor (EPOR) in erythrocyte precursor cells, causing them to differentiate into mature erythrocytes that are released into circulation. As the oxygen-carrying capacity of the blood increases, secretion of EPO by the kidneys decreases. Neurons in the CNS also express EPOR, and EPO has been shown to decrease apoptosis of both erythrocyte precursor cells and CNS neurons. EPO also promotes angiogenesis, the production of new blood vessels. The human EPO gene has been cloned and expressed in vitro. The recombinant gene product (rHuEPO) is frequently administered to patients who have anemia resulting from either kidney failure or chemotherapy. More recently, it has been shown that a significant number of tumors express EPOR, even though the healthy tissue from which the tumor was derived does not. Experiments in mice indicate that EPO prevents apoptosis and increases angiogenesis in at least some types of EPOR-positive tumors. Interested in developing ways to treat human strokes, researchers are attempting to develop forms of EPO that act on CNS neurons without affecting erythrocyte production in the bone marrow. One benefit of such a form of EPO in stroke treatment would be to: O A. promote apoptosis of damaged CNS neurons without affecting blood oxygen levels. O B. limit neuronal cell death without causing an immediate decrease in the oxygen-carrying capacity of the blood. O C. prevent apoptosis in the CNS without causing a harmful increase in blood viscosity. O D. promote healing in the CNS without increasing the risk of developing tumors.