In immunoblotting, p-H2AX was increased in the irradiated group; therefore, DNA damage was considered to be induced in endometrial cancer cells; p-Chk1, p-ATM, and p-Chk2 were increased in the irradiated group, which indicated that the ATR-Chk1 and ATM-Chk2 pathways were activated in response to DNA damage. The gene discussed is CHEK1; the disease is endometrial cancer.