Apoptosis is a series of controlled sequential events resulting in cell death. This complements proliferation in the maintenance of tissue homeostasis. The process is regulated to give a “shrinking cell” with a charactertstic appearance. Apoptotic cells undergo compaction of nuclear chromatin and cytoplasmic condensation followed by budding of the cell to form membrane bound apoptotic bodies (1 , 2 ). These contain varying proportions of cellular organelles and nuclear material and are rapidly phagocytosed by surrounding cells. Cell loss, therefore, is achieved without the induction of inflammation. The discovery that certain proto-oncogenes (3 ), e.g., c-myc and bcl-2 and the tumor suppressor gene p53 are implicated in the control of apoptosis has focused attention on both the role of apoptosis in tumorogenesis and as a possible pathway to which cancer therapeutic regimens could be directed (4 ). The latter point is clinically relevant in that radiotherapy, hormone therapy, and a broad spectrum of chemotherapeutic agents all induce apoptotic death in target cells. Therefore, tumor resistance to these agents may well be associated with blockades or lesions in the apoptotic pathway.