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Apoptosis is regulated by opposing survival and death signals. In the intrinsic pathway, the balance of BCL-2 family proteins controls mitochondrial permeabilization and cytochrome c release, which leads to apoptosome formation and caspase activation. The extrinsic pathway begins when death receptors recruit signaling proteins that activate caspases. p53 can promote apoptosis or cell-cycle arrest, while inhibitors of apoptosis can restrain caspase activity. Cell-cycle progression through G1, S, G2, and M depends on cyclin-CDK complexes and checkpoints. Regulators such as Rb, E2F, CDK inhibitors, and ATM/ATR help respond to growth signals or DNA damage. Cancer-associated changes can weaken these safeguards; the lesson also connects these mechanisms with therapeutic targets.