Apoptosis is the descriptive name given to the process of programmed cell death in vertebrates. During apoptosis, a cell activates an intrinsic suicide mechanism that systematically trashes the cell: its surface membrane begins to bleb and express pro-phagocytic signals, the cell shrinks and severs contact with its neighbors, chromatin becomes condensed and cleaved (ensuring genetic death of the affected cell), and eventually the whole cell fragments into membrane-bound vesicles that are rapidly ingested by neighboring cells. The apoptotic process is extremely rapid (typically between a few minutes and a few hours), and the apoptotic debris is cleared with similar rapidity.

Up until some 4 years ago, apoptosis held much the same status among serious scientists as aromatherapy does among physicians—an interesting and amusing concept, decorative, but definitely not mainstream. Of course, all that has now changed. Nowadays, the ferocious pace (and funding) of research into apoptosis is matched only by a deep sense of frustration that, despite elucidation of many of the important players in the cell death process, very little hangs together to give a coherent picture of how apoptosis is regulated and executed. Part of the problem is that almost everything (for example, oncoproteins, tumor suppressor proteins, growth factors, and signaling pathways) seems able to induce apoptosis and almost everything (for example, oncoproteins, tumor suppressor proteins, cytokines, and signaling pathways) seems able to suppress it. Nonetheless, despite the wide diversity and dissimilarity of factors that can modulate apoptosis, the basal apoptotic mechanism appears to be relatively simple in general structure and highly conserved throughout metazoan evolution. It is therefore difficult to see how so many different kinds of stimulus and insult, in so many diverse organisms, can be wired into one unitary suicide machine.