accidental injury, they undergo a traumatic death, swelling and bursting and flooding their surroundings with their internal components. The area then becomes inflamed as the body cleans up this necrotic mess. But cells may also undergo a controlled, antiseptic death termed “apoptosis” or “programmed cell death.” When given the signal, a cell will shut down its major regulatory and homeostatic systems, it will disassemble its internal infrastructure, and it will fragment itself into neat, bite-size pieces ready to be consumed by neighboring cells. All cells are primed with this “cyanide pill,” ready to commit suicide at a moment’s notice. Apoptosis is used throughout development of higher animals, as cells are patterned within the embryo. In adults, obsolete cells are given the signal to die, and rogue cells damaged by radiation or viral infection are destroyed cleanly by apoptosis. Caspases (Fig. 1) are the executioners of apoptosis. Caspases are cysteine proteases, using the sulfur atom in cysteine to cleave polypeptide chains. Caspases are not indiscriminant proteases, however. They search for a specific sequence in their target proteins, typically cleaving solely next to aspartate amino acids (thus the name “caspase”: “c” for cysteine protease and “asp” for the strong aspartate preference). The targets of caspases are carefully planned, like charges planted during a building demolition, to allow the ordered destruction of the cell. Regulatory proteins such as Rb (retinoblastoma protein) are cleaved, halting cell-cycle progression, and nucleic acid synthesis is halted by destruction of polymerases. Major homeostatic and repair mechanisms are disabled by cleavage of key enzymes. Structural proteins, such as cytoplasmic actin and nuclear lamins (Fig. 2), are specifically disassembled. DFF (DNA fragmentation factor) is activated, leading to fragmentation and condensation of the cell’s genetic material. And finally, to facilitate rapid recycling, adhesion proteins are cleaved, releasing the cell from the surrounding tissue, and the lipids in the cell membrane are subtly changed, signaling to neighboring cells that the apoptotic cell is fair game. Tumor growth is the result of a deadly combination: a mutation in cyclin or another gene controlling the cell cycle, which removes the normal restraints on growth, combined with a mutation in apoptosis, which disables the system that normally catches these abnormally growing cells. As well as removing the means to destroy rapidly growing tumor cells, faulty apoptosis also confers resistance against many major medical treatments. Chemotherapy and radiation therapy kill cancer cells not by producing necrotic The Molecular Perspective: Caspases