In most tissues, cell division occurs continuously, without an increase in organ size or tumor development, suggesting that the rate of division is balanced by the rate of cell death. This balance is maintained by programmed cell death, or apoptosis (1). In contrast to necrotic cell death, apoptosis follows a stereotypical pattern of morphologic changes, irrespective of the initiating evcnt. These changes include membrane ruffling, cytoplasmic and organelle condensation/shrinkage, nuclear contraction, and DNA cleavage. The resulting cellular fragments, or apoptotic bodies, are subject to rapid receptor-mediated ingestion by neighboring cells and resident tissue phagocytes. It is thought that phagocytes are not activated on ingestion of these bodies, and apoptosis usually occurs without the inflammatory changes which accompany necrosis (2). Apoptosis occurs in a variety of specific physiologic situations, including embryogenesis, and plays a crucial role in normal tissue homeostasis. It can be induced by a specific ligand-receptor interaction (eg, Fas ligand [Fas-L]/Fas, tumor necrosis factor (Y [TNFa]/TNF receptor 1 [TNFRl]), signal withdrawal (eg, growth factor deprivation), or an innate cell program (eg, in the neutrophil). A breakdown in the delicate balance between cell survival and apoptosis has been implicated in the pathogenesis of a number of rheumatic diseases (Figure 1).