The uncapped telomeres and double-strand DNA breaks activate the DNA damage response (DDR) that stabilizes p53 through posttranslational phosphorylation via ATM (ataxia-teleangiectasia, mutated) and ATR (ATM and Rad3-related) serine/threonine protein kinases [22] or by blocking the degradation of p53 via p14ARF (a tumor suppressor)-mediated inhibition of the MDM2 (mouse double minute 2) ubiquitin ligase [23]. The gene discussed is ATM; the disease is neoplasm.