The analyses of Li-Fraumeni patients with inherited TP53 mutations as well as mouse Li-Fraumeni models consequently demonstrate that the increased tumor development in Li Fraumeni syndrome involves selective pressure to eliminate the activity of the wt TP53 allele from the heterozygous setup with mutant TP53. It is achieved via a loss-of-heterozygosity (LOH) and other mechanisms of wt p53 inactivation in Li-Fraumeni patients [66, 67] and mouse models [21]. The gene discussed is TP53; the disease is Li-Fraumeni syndrome.