CHEK2 and neoplasm: This concept, which we have later extended also to brain tumors [56, 57] and MLL-ENL oncogene-induced leukemogenesis [58], furthermore explains the disease-evolutionary pressure to select for inactivating mutations in checkpoint genes such as TP53, ATM or CHK2 [53–55, 59], as secondary events that allow checkpoint bypass and tumor cell proliferation, at the expense of high genomic instability.