Our research examines gene-directed programs that specify programmed and ‘unprogrammed’ cell death. In both vertebrates and invertebrates, dying cells often progress through a series of ultrastructural changes referred to as apoptosis. Stimuli that provoke apoptosis have been extensively investigated in numerous experimental models and it is well established that this form of programmed cell death requires genetic functions within the dying cell (see movie tutorial). Apoptosis is important not only for development but also as an adaptive response during cellular injury and in viral infection. Consistent with this, extensive evidence links aberrant apoptosis to the etiology of cancer, neurodegenerative disorders, auto-immunities, AIDS and heart disease. Prompted by the cloning of ‘CED genes’ necessary for PCD in the nematode, our collective understanding of apoptotic cell death has grown at an astonishing pace since the early 1990s. Family members homologous to CED genes were found in diverse animal models, establishing that core components of the "apoptotic engine" are highly conserved. Despite our advanced body of knowledge, fundamental gaps in our understanding of apoptotic death in biology and medicine remain. An emerging literature also supports the view that other forms of cell suicide occur and, like apoptosis, these alternate forms of cell death may also be controlled through genetically encoded programs.