Cell death is a critical process in multicellular organisms, maintaining tissue homeostasis and eliminating potentially harmful cells. There are three major types of cell death: apoptosis (type I), autophagic cell death (type II), and necrosis (type III). Each type is initiated through distinct signaling pathways, which can overlap. **Apoptosis** is triggered by death receptors (e.g., Fas) bound by their ligands or by Bcl2-family proapoptotic proteins causing mitochondrial outer membrane permeabilization. Both pathways lead to caspase activation, which dismantles the cell. Caspases are cysteine proteases that cleave intracellular proteins, leading to characteristic morphological changes such as cell shrinkage, membrane blebbing, and chromatin condensation. **Autophagy** is a catabolic process where parts of the cytosol and organelles are engulfed by autophagosomes and degraded. While primarily a survival mechanism, autophagic cell death has been observed in certain conditions, such as during Drosophila metamorphosis and deregulated H-Ras activity. **Necrosis** is characterized by rapid loss of plasma membrane integrity and can result from active signaling pathways, such as the RIP3-dependent pathway, which is activated by various stimuli including DNA damage and viral infections. The chapter delves into the detailed mechanisms of apoptosis, including the roles of caspases, the mitochondrial pathway, and the death receptor pathway. It also discusses the regulation of caspase activation by kinases and the involvement of autophagy in cell death, highlighting cases where autophagy actively promotes cell death.Cell death is a critical process in multicellular organisms, maintaining tissue homeostasis and eliminating potentially harmful cells. There are three major types of cell death: apoptosis (type I), autophagic cell death (type II), and necrosis (type III). Each type is initiated through distinct signaling pathways, which can overlap. **Apoptosis** is triggered by death receptors (e.g., Fas) bound by their ligands or by Bcl2-family proapoptotic proteins causing mitochondrial outer membrane permeabilization. Both pathways lead to caspase activation, which dismantles the cell. Caspases are cysteine proteases that cleave intracellular proteins, leading to characteristic morphological changes such as cell shrinkage, membrane blebbing, and chromatin condensation. **Autophagy** is a catabolic process where parts of the cytosol and organelles are engulfed by autophagosomes and degraded. While primarily a survival mechanism, autophagic cell death has been observed in certain conditions, such as during Drosophila metamorphosis and deregulated H-Ras activity. **Necrosis** is characterized by rapid loss of plasma membrane integrity and can result from active signaling pathways, such as the RIP3-dependent pathway, which is activated by various stimuli including DNA damage and viral infections. The chapter delves into the detailed mechanisms of apoptosis, including the roles of caspases, the mitochondrial pathway, and the death receptor pathway. It also discusses the regulation of caspase activation by kinases and the involvement of autophagy in cell death, highlighting cases where autophagy actively promotes cell death.