It is important to note that altered Trp53 expression is not always sufficient to rescue embryonic lethality in mice; for example, PLK1-interacting checkpoint helicase (PICH)-deficient mice possess developmental defects in the presence or absence of p53 [36], and ATR mutants (Seckel syndrome) are not completely rescued from embryonic lethality with the inactivation of Trp53 [37]. Here, ATR is linked to Seckel syndrome.