This review article by Mohamed Hassan et al. discusses the role of apoptosis in cancer and the molecular targeting therapies that can be used to stimulate apoptosis in cancer cells. Apoptosis, or programmed cell death, is crucial for maintaining genomic integrity and homeostasis in normal cells. Defects in apoptosis can lead to cancer or autoimmunity, while enhanced apoptosis can cause degenerative diseases. The apoptotic signals are complex and regulated at multiple levels, including the inhibition of apoptosis by inhibitor of apoptosis (IAP) proteins and FLICE-inhibitory protein (c-FLIP). Cancer cells often use various molecular mechanisms to suppress apoptosis, such as overexpressing antiapoptotic proteins like Bcl-2 or downregulating proapoptotic proteins like BAX. The article reviews the main regulatory molecules that govern the extrinsic and intrinsic pathways of apoptosis in normal cells and how carcinogenesis can be developed via defective apoptotic pathways. The authors also discuss promising cancer treatment strategies that target apoptotic inhibitors, including Bcl-2 family proteins, IAPs, and c-FLIP, to induce apoptosis. They highlight the development of novel therapeutics that prime the apoptotic machinery to act as apoptosis-inducing agents, which can be used alone or in combination with conventional therapies. Specific examples of these strategies include targeting Bcl-2 family members, modulating cell cycle control systems, and using cyclines and Ku70 to enhance apoptosis. Overall, the article provides a comprehensive overview of the molecular mechanisms of apoptosis and the potential of targeted therapies to overcome resistance to apoptosis in cancer cells.This review article by Mohamed Hassan et al. discusses the role of apoptosis in cancer and the molecular targeting therapies that can be used to stimulate apoptosis in cancer cells. Apoptosis, or programmed cell death, is crucial for maintaining genomic integrity and homeostasis in normal cells. Defects in apoptosis can lead to cancer or autoimmunity, while enhanced apoptosis can cause degenerative diseases. The apoptotic signals are complex and regulated at multiple levels, including the inhibition of apoptosis by inhibitor of apoptosis (IAP) proteins and FLICE-inhibitory protein (c-FLIP). Cancer cells often use various molecular mechanisms to suppress apoptosis, such as overexpressing antiapoptotic proteins like Bcl-2 or downregulating proapoptotic proteins like BAX. The article reviews the main regulatory molecules that govern the extrinsic and intrinsic pathways of apoptosis in normal cells and how carcinogenesis can be developed via defective apoptotic pathways. The authors also discuss promising cancer treatment strategies that target apoptotic inhibitors, including Bcl-2 family proteins, IAPs, and c-FLIP, to induce apoptosis. They highlight the development of novel therapeutics that prime the apoptotic machinery to act as apoptosis-inducing agents, which can be used alone or in combination with conventional therapies. Specific examples of these strategies include targeting Bcl-2 family members, modulating cell cycle control systems, and using cyclines and Ku70 to enhance apoptosis. Overall, the article provides a comprehensive overview of the molecular mechanisms of apoptosis and the potential of targeted therapies to overcome resistance to apoptosis in cancer cells.