In principle, mutations that selectively retain the pro-proliferative or survival functions of wild type p53 (e.g. adaptation to metabolic stress) while disrupting the canonical tumor suppressive activities (e.g. apoptosis, senescence) might produce phenotypes that appear similar to a GOF (Table 1) (refs. [7, 37, 41]). The gene discussed is TP53; the disease is neoplasm.