The p53 tumor-suppressor gene plays a crucial role in the cellular response to stress (reviewed by Vogelstein et al. [1 ]). Under normal conditions, p53 is rapidly degraded and thus is not present in detectable levels within the cell. A variety of cellular stresses, including DNA damage and oncogene activation, result in stabilization and activation of p53, causing the protein to accumulate within the nucleus. Stabilized p53 then transcriptionally activates the expression of a variety of proteins that are involved in cell-cycle regulation and apoptosis. The damaged cells may then undergo cell-cycle arrest, allowing them to repair the genetic damage. Alternatively, if the damage is irreparable, the p53 protein initiates a cascade of events that culminate in programmed cell death (apoptosis) (2 ).