These findings are consistent with previous researches that show that the inhibition of CHK1 can increase the activity of various DNA damage or DNA synthesis inhibition therapies in different cancer cells.30–35 As is well known, the DNA Damage Response (DDR) signaling pathway includes the ATM/ATR-CHK1/CHK2-Cdc25s pathway (for rapid, reversible reactions) and the p53-dependent pathway (for slower, irreversible reactions).36 P53 is a central downstream checkpoint signaling protein responsible for apoptosis response. This evidence concerns the gene CHEK2 and cancer.