In mammals, CtIP is the primary factor responsible for cell-cycle regulation of resection19,20,22. This is accomplished by two types of cell-phase-specific post-translational modifications of CtIP. First, CtIP protein levels are suppressed in G1 by proteasome-mediated degradation, which is alleviated as cells enter S phase, thereby permitting a rise in protein levels23. Second, CtIP is a substrate for S-phase-specific CDK activity19,22,24. This phosphorylation is required for assembly of the MRN–CtIP–BRCA1 resection complex20,22.