Given the stunted half-life of around 30 min for p53, these acetylations have been reported to impart stability to p53, which then mediates a range of downstream functions in response to DNA damage, oncogenic stress, age-associated abnormalities, tumor suppression and others (Donehower, 2009; Lozano, 2010; Vousden and Prives, 2009). This evidence concerns the gene TP53 and neoplasm.