As a mechanism of cell death, apoptosis is very distinct from necrosis: whereas apoptosis is a deliberate process modulated by specific genetic pathways, necrosis can be considered accidental, as when a toxin blocks cellular functions necessary for survival (2). Morphologically, the cell undergoing apoptosis is characterized by a reduction in cell volume, while the chromatin becomes pyknotic and condensed into delineated fragments associated with the nuclear envelope. Nuclear condensation during apoptosis can be detected by microscopy approaches, especially confocal laser scanning microscopy. The nuclear chromatin in the apoptotic cell then condenses, typically followed by a loss of the nuclear membrane and fragmentation of the nuclear DNA into discrete, 180 to 200-bp fragments (3). When run on a gel, the fragments are distributed in a periodic fashion, referred to as “DNA laddering.” The DNA breaks associated with apoptosis can be visualized by microscopy following terminal deoxynucleotide transferase-mediated dUTP-biotin nick end labeling (TUNEL) and in situ end labeling (4). TUNEL approaches are commonly used in combination with other techniques (microscopy, gel electrophoresis) to demonstrate apoptosis, because necrotic cells have also been shown, at times, to stain with this technique (5). In addition to DNA fragmentation, apoptosis is characterized by condensation of the cytoplasm, elimination of microvilli, and cell-surface blebbing. In the latter stages of apoptosis, prominent surface protrusions eventually separate and form sealed plasma membrane vesicles; the entire cell is thus reduced to microscopic bodies of various size and content that are efficiently eliminated by parenchymal cells and mononuclear phagocytes without generally triggering an immunologic response. Thus, apoptosis is very distinct from necrosis, as reviewed in (Table le1).