Cellular systems with a high intrinsic proliferative capacity and cell turnover in the body such as hematopoietic cells are in constant need to control cell numbers (1,2). Thus, an excess of precursor cells is produced daily, which mature into effector cells. In the lymphoid system, the vast majority of T- and B-cell precursors die by a default mechanism because of the inefficient production of functional antigen receptors. Apoptosis is also a key mechanism for the termination of an immune response by elimination of unnecessary effector cells to avoid autoimmunity and tissue damage. In the myeloid system, a large number of granulocytes are produced per day, which disappear in the peripheral tissues by a process that at least in vitro involves spontaneous apoptosis. From this intrinsic capacity of hematopoietic cells to undergo apoptosis, it is obvious that too much apoptosis or not enough apoptosis will lead to hematopoietic failure, uncontrolled lymphoproliferation with autoimmunity or leukemia and lymphoma.