Aoptosis, or programmed cell death, is a genetically encoded cell suicide program defined by characteristic morphologic, biochemical, and molecular changes resulting in nonpathologic cell loss. A large number of distinct cellular phenotypes set apoptosis apart from another cell death process, i. e., necrosis.^1,2 Apoptosis plays a key role in physiological processes such as embryonic development, maturation of the host immune system, and in maintaining tissue and organ homeostasis. Apoptosis has also been implicated in a variety of pathological conditions exemplified by cardiac infarction, atherosclerosis, Alzeimer’s disease and other neurodegenic diseases, HIV, tumorigenesis and tumor progression. A multitude of factors have been implicated in regulating/modulating apoptosis; these include: (i) oncogenes/tumor suppressor genes exemplified by p53, bcl-2 family (bcl-2, bcl-XL, bcl-Xb, bcl-XS, bax, BAG-1, bad, bak, Al, Mcl-1), myc, ras, abl, raf, Rb-1, and Waf-1; (ii) growth factor/growth factor receptors represented by NGF/NGF receptor, TNF-α/Fas, TGF-β/TGF receptor, IGF-1/IGF receptor, and PDGF/PDGF receptor; (iii) intracellular signal transducers such as protein kinase C, tyrosine kinases and protein phosphatases, lipid signaling molecules such as ceramide, and Ca²⁺; (iv) cell cycle regulators exemplified by cdc-2 and E2F; (v) reactive oxygen species; (vi) extracellular matrix regulators/signal transducers (extracellular matrix proteins such as fibronectin and transmembrane integrin receptors); (vii) specific endonucleases such as Ca²⁺- and Mg²⁺-dependent DNase; and (viii) cytoplasmic proteases typified by ICE (interleukin 1-converting enzyme) family.^1–10 The major impact of apoptosis on cancer research is manifested primarily in three areas: oncogenesis, tumor homeostasis, and the mechanism of action of c ytotoxic antitumor drugs.¹¹ Most anti-tumor agents such as radiation (by generating oxygen radicals) and chemotherapeutic drugs kill tumor cells by inducing apoptosis. Likewise, development by tumor cells of resistance to these treatments is mostly a result of loss of response to apoptosis induction.^1,11