TP53 and cancer: Our model also predicts that the selective pressure of cancer has either led to the “architectural” evolution of epithelial proliferative units with large numbers of stem cells and virtually no metapopulation dynamics (Clayton et al., 2007), or small numbers of stem cells within each proliferative unit, with frequent expansions of clones with fitness advantages, as is seen in p53 mutant clones the skin (Chao et al., 2008; Zhang et al., 2005).