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. This evidence concerns the gene CHEK2 and neoplasm.