These evidences support the mitotic lethality rationale that cancers deficient in functional p53, a key component of the G1-S checkpoint, are more reliant on the G2-M checkpoint to repair DNA damage, and that abrogation of the G2-M checkpoint by WEE1 inhibition sensitizes p53-deficient cells to DNA-damaging agents [166] (Fig. 3B). This evidence concerns the gene TP53 and cancer.