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Apoptosis, first identified in the 1970s, was initially perceived as a process comparable to mitosis. Commonly referred to as programmed cell death, it plays an essential role in maintaining a balance with mitosis by regulating cell populations during development, preserving tissue homeostasis in adults, and contributing to various biological processes.[1] Over time, apoptosis was more clearly defined as a genetically programmed, ATP-dependent, enzyme-driven mechanism that eliminates cells deemed unnecessary or potentially harmful to the organism.[2] Apoptosis results when the cytoskeleton is broken down by proteases and DNA is degraded by endonucleases through several pathways that are homeostatic or pathological. The process maintains homeostasis when cells compromise the organism's survival, but apoptosis does not occur at the appropriate rate or in the correct sequence when the process is no longer regulated.[3] Caspases mediate the process through the downstream effects of the upstream activation by intrinsic and extrinsic pathways, either working separately or simultaneously.[4]