Claspin over-expression not only guarantees the availability of FPC to stabilize and restart stalled replication forks and allow DNA replication and cell division, but also permits tumor cells that can activate Chk1-mediated checkpoint responses (Figure 2, bottom), providing the cell time to repair DNA damage and survive, or to escape senescence induction or apoptosis [94,109,110]. Here, CLSPN is linked to neoplasm.