Loss of the wild-type p53 allele (loss of heterozygosity (LOH); p53m/+ ➔ p53m or m/m) is an important step during tumorigenesis in p53 heterozygous mutant humans (Li Fraumeni Syndrome) and animals (zebrafish and mouse p53 knockouts) [20,22,46–51]; therefore we postulated that esco2 heterozygosity may enhance tumor formation in a p53 heterozygous animal by accelerating p53 LOH. This evidence concerns the gene TP53 and Li-Fraumeni syndrome.