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described by Kerr and colleagues in 1972 [3]. Moreover, the activation of caspase proteases is a hallmark of this form of cell death [4]. The death receptor route and the mitochondrial pathway are the two main signaling mechanisms that initiate apoptotic cell death. The second type of contact contains the traditional ligand-cell­surface-receptor triangle. One member of the tumor necrosis factor receptor (TNFR) family, cytotoxic lymphocytes (CTLs), expresses ligands for death receptors (DRs), which allow them to kill altered or contaminated cells. Assuming the target cells have these DRs, these ligands cause them to undergo apoptotic cell death. Immune system homeostasis and function depend on DR-induced cell death in general. The mitochondrial apoptotic pathway, on the other hand, is typically begun by the cell itself. When cells are irreparably damaged, apoptosis is actively engaged by the majority of cellular stressors, including DNA damage (caused by genotoxic chemi­cals or DNA repair errors) and endoplasmic reticulum (ER) stress (caused by the buildup of unfolded proteins). Furthermore, cell death can occur in the absence of a signal, such as those activated by growth factors (such as cytokines and neuro­trophic factors). The procedure is predicted to kill half of the neurons created, although it is crucial for vertebrates’ nervous system development [5]. A lack of neurotrophic factor stimulation, which occurs when some neuronal progenitors do not migrate or innervate their targets correctly, contributes to this cell death. In the same way, the rapid reduction of the lymphocyte number following pathogen clear­ance is caused by cytokine deprivation in conjunction with the DR pathway during an immunological response. Another type of cell death caused by “loss-of-signal” is anoikis, which happens when cells in the cell membrane (epithelial or endothelial cells) separate from the Extracellular Matrix (ECM).Here, apoptosis results from the loss of pro-survival signaling pathways induced by unligated integrin family ECM receptors. This process stops cells that have shed from their initial site from spreading to other areas, which is a hallmark of cancer cells that have metastasized. As a last line of defense against cancer, oncogenes (like Myc) can trigger cell death. When oncogene overexpression or mutation triggers abnormal mitogenic signals, a p53-dependent apoptotic pathway is activated and helps to regulate this process. Thus, it is frequently necessary to avoid apoptotic cell death in order to maintain oncogene transformation [6].