Nitric oxide (NO) or related molecules of both endogenous and exogenous origin inhibit programmed cell death in a variety of cells and tissues. This general protective function is largely independent of the apoptotic stimulus. S-nitrosylation of the catalytic-site cysteine of caspases is a well-established and possibly widespread mechanism of enzyme inhibition that protects from cell death. However, NO may inhibit apoptosis by additional mechanisms. The physiological and pathological significance of NO's anti-apoptotic activity remains to be determined in most cases.