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The tumor suppressor p53 is a transcriptional master regulator that promotes DNA repair, cell cycle arrest, senescence, and apoptosis in re-sponse to challenges to genomic integrity, thereby guarding against oncogenesis (Junttila and Evan, 2009; Vousden and Prives, 2009). Maintained at low levels in the steady-state by proteasomal degradation, p53 is rapidly stabilized and acti-vated in response to DNA damage and a variety of other metabolic stressors (Lavin and Gueven, 2006). In addition to classical genotoxic stress (e.g., -irradiation), p53 is also responsive to in-flammatory stressors such as TNF (Donato and Perez, 1998) and reactive oxygen species (ROS; Lavin and Gueven, 2006; Vousden and Prives, 2009) and is up-regulated at sites of inflamma