TP53 and neoplasm: In the cell-cycle checkpoint control, active CHEK2 and other DNA damage-triggered protein kinases stabilize TP53 or speed up Cdc25A degradation through the coordination of DNA repair, cell-cycle progression, and death (Matsuoka et al., 1998; Hirao et al., 2000; Falck et al., 2001; Zannini et al., 2014) The tumor-suppressing function of the cell cycle regulator CHEK2 is mediated via homologous recombinant DNA repair, and genetic changes in it render malignancies susceptible to more advanced targeted therapies.