Bcl-2 was the first recognized component of the physiological cell death mechanism. It belongs to an expanding family of proteins that regulate apoptosis during development and homeostasis. Experiments using transgenic and gene knockout mice have revealed much about the roles played by Bcl-2, Bcl-x and Bax in regulating apoptosis in the immune system. Genetic data from C. elegans have shown that Bcl-2 like proteins ultimately determine whether a set of apoptosis effector cysteine proteases becomes activated in response to a death signal. How Bcl-2 and its relatives achieve this regulation remains unknown.