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Molecular Toxicology Laboratories, Division of Pharmaceutical Sciences, Arnold & Marie Schwartz College of Pharmacy & Health Sciences, Long Island University, Brooklyn, NY 11201.It is an interesting paradox that cell life is dependent on cell death, and mitochondria stands at the crossroads of cell life and cell death because of its ability to micromanage oxidative stress, directly and/or indirectly influence genome-dependent and genome-independent events, regulate intracellular micro and macromolecular functions, and allow or resist conditions for cyt c release.If all these perturbations succeed, they ultimately articulate pathological consequences in various tissues.Oxidative stress manipulates mitochondrial membrane to form transition pores for flooding Cyt c into the cytosol, alter electron transport chain to jeopardize ATP production, perturb ion homeostasis via Ca2+ deregulatation, tilt redox balance and slither GSH concentration to accomplish its death inducing goals, whereas at the genetic level, mitochondrial membrane bound Bcl-2 family members become pro-active during such perturbations to antagonize death mission.