Apoptosis is a regulated cellular process critical in both physiological and pathological conditions. It plays a key role in disease pathogenesis, with imbalances in apoptosis contributing to conditions like cancer. In cancer, insufficient apoptosis allows malignant cells to survive. Apoptosis involves complex pathways, including intrinsic (mitochondrial) and extrinsic (death receptor) pathways, and defects in these can lead to cancer progression and drug resistance. Despite its role in disease, apoptosis is a major target for cancer treatment, as targeting it can induce cell death in malignant cells. The Bcl-2 family of proteins regulates apoptosis, with pro-apoptotic and anti-apoptotic members balancing cell death. Mutations in p53, a key tumor suppressor, are linked to many cancers, as it promotes apoptosis and cell cycle control. Inhibitor of apoptosis proteins (IAPs) also regulate apoptosis, and their dysregulation contributes to cancer. Targeting these proteins with drugs or therapies can restore apoptosis and inhibit tumor growth. Caspases are central to apoptosis, and their dysfunction can lead to cancer. Targeting caspases or their regulators can enhance apoptosis in cancer cells. Various strategies, including BH3 mimetics, siRNA, and small molecule inhibitors, are being explored to target apoptotic pathways. These approaches aim to restore normal apoptosis and improve cancer treatment outcomes. Clinical trials are testing new molecules targeting apoptosis, including inhibitors of Bcl-2 family proteins and IAPs. While promising, these treatments must be carefully evaluated to avoid unintended effects on normal cells. Overall, targeting apoptosis offers a potential therapeutic strategy for cancer, but challenges remain in ensuring safety and efficacy.Apoptosis is a regulated cellular process critical in both physiological and pathological conditions. It plays a key role in disease pathogenesis, with imbalances in apoptosis contributing to conditions like cancer. In cancer, insufficient apoptosis allows malignant cells to survive. Apoptosis involves complex pathways, including intrinsic (mitochondrial) and extrinsic (death receptor) pathways, and defects in these can lead to cancer progression and drug resistance. Despite its role in disease, apoptosis is a major target for cancer treatment, as targeting it can induce cell death in malignant cells. The Bcl-2 family of proteins regulates apoptosis, with pro-apoptotic and anti-apoptotic members balancing cell death. Mutations in p53, a key tumor suppressor, are linked to many cancers, as it promotes apoptosis and cell cycle control. Inhibitor of apoptosis proteins (IAPs) also regulate apoptosis, and their dysregulation contributes to cancer. Targeting these proteins with drugs or therapies can restore apoptosis and inhibit tumor growth. Caspases are central to apoptosis, and their dysfunction can lead to cancer. Targeting caspases or their regulators can enhance apoptosis in cancer cells. Various strategies, including BH3 mimetics, siRNA, and small molecule inhibitors, are being explored to target apoptotic pathways. These approaches aim to restore normal apoptosis and improve cancer treatment outcomes. Clinical trials are testing new molecules targeting apoptosis, including inhibitors of Bcl-2 family proteins and IAPs. While promising, these treatments must be carefully evaluated to avoid unintended effects on normal cells. Overall, targeting apoptosis offers a potential therapeutic strategy for cancer, but challenges remain in ensuring safety and efficacy.