Whereas these functions point towards a tumor suppressor role for CHK1, mouse models modulating ATR-CHK1 expression and genetic evidence from human tumors suggest otherwise: Atr and Chk1 knock-out models do not display higher tumor frequency; Chk1 favors oncogene-induced transformation in mice; CHK1 is frequently overexpressed in human cancers, while loss-of-function mutations are rare [2, 3]. Here, ATR is linked to cancer.