Studies from Khanna et al., suggest that because the CHK1-CIP2A-PP2A pathway is driven by DNA-PK activity, functioning regardless of p53 or ATM/ATR status, which may (1) explain how CHK1 inhibitors mediate single-agent anticancer efficacy and (2) define CIP2A-PP2A status in cancer cells as a pharmacodynamic marker for the response to CHK1-targeted therapy [23]. This evidence concerns the gene CIP2A and cancer.