Claspin may generally act as a tumor suppressor, its mutation/inactivation having the potential to act as a driver mutation in cancer development, but its over-expression may also act as a secondary event that can correlate with a poor prognosis, or, in specific contexts, can amplify driver mutation events of given types of cancer (e.g., TP53 mutation, HER2 over-expression). Here, CLSPN is linked to neoplasm.