ATM and breast cancer: This effect can be explained by known mechanisms involving interactions between BRCA1, ATM and TP53 (Xu et al, 1999; Gatei et al, 2000; Wang, 2000; Khanna and Jackson, 2001), including (i) ATM serves as the upstream sensor and, upon DSB formation, phosphorylates BRCA1 and TP53 to trigger DSB repair and cell cycle regulation and (ii) for breast cancer formation, breast epithelium cells that are genomically unstable because of defective BRCA1-associated repair also need to undergo checkpoint inactivation (such as ATM or TP53) in order to escape checkpoint surveillance.