Cell death is an important process to cell homeostasis, response to pathogens, and for the effectiveness of chemotherapeutic drugs. There are several cell death pathways that have been discovered and each are involved either in specialized cells or in response to a specific response to stress or insult. Each of these pathways is associated with a unique cell morphology and a specific set of genes. Apoptosis may be divided into the intrinsic and extrinsic pathway. The intrinsic pathway involves disruption of the mitochondrial membrane and the release of cytochrome C. The extrinsic pathway is activated from the cell surface through a family of death receptors. Autophagy is a process in which the cell can remove any unnecessary or damaged components. Ferroptosis, which is a type of cell death that is dependent upon iron and is characterized by the accumulation of lipid peroxides. Necroptosis involves receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and is manifested by morphological features of necrosis. Pyroptosis is an inflammatory form of cell death triggered by inflammasomes, which results in the cleavage of gasdermin D (GSDMD) and activation of inactive cytokines like IL-18 and IL-1β. NETosis involves the formation of neutrophil extracellular traps (NETs) consisting of modified chromatin decorated with bactericidal proteins from granules and the cytoplasm. Entosis is a cannibalistic process in which a cell invades or is engulfed by another cell. Methuosis is characterized by the accumulation of cytoplasmic vacuoles derived from macropinosomes and late endosomes, followed by metabolic failure and rupture of the plasma membrane. Parthanatos is a PARP1-dependent, caspase-independent, cell death pathway that is distinct from apoptosis, necrosis, or other known forms of cell death. The Pan Cell Death Primer Library contains primer sets that amplify the prominent genes that are associated with these pathways.