This was supported by the findings from wrn-knockout mice studies in which knockout of wrn alone did not lead to WS phenotype while crossing wrn-knockout mice with p53-null mice or mice carrying a null mutation in the terc gene, resulted in classic WS phenotypes: premature death, rapid tumorigenesis, etc. [20], [21], [22], [23]. The gene discussed is WRN; the disease is Werner syndrome.