Some p53 mutants such as p.R175P are defective in activating genes associated with apoptosis without impairing growth arrest.71 Onset of tumors in knock-in mice expressing this mutant (p.R172P in mice) is delayed compared with TP53−/− mice or mice expressing hotspot mutations.72 In contrast to tumors expressing other p53 mutants, these tumors were mostly diploid, indicating that the growth arrest function of TP53 could be essential for maintaining genetic stability, but is not the primary tumor suppressor function of wild-type TP53. The gene discussed is TP53; the disease is neoplasm.