While chronic activation of p53‐dependent apoptosis and cell cycle arrest/cellular senescence programs by uncapped telomeres is potently tumor suppressive, we have previously shown that an undesirable consequence of Pot1b deletion is compromised stem cell proliferation, resulting in systemic multi‐organ failure and the onset of premature aging phenotypes, presumably due to activation of p53‐dependent proliferative checkpoints (Wang et al., 2011, 2013). Here, TP53 is linked to neoplasm.