This finding corroborates observations in glioma cells with DNA-PKcs deficiency and in M059K cells transfected with DNA-PKcs siRNA (Fig. 4b and d) and indicates tumor evolution shifts caused by enhanced interaction between FEN1 and replisomes in cases of DNA-PKcs deficiency and FEN1 contributes to structured replisomes during cell circle. The gene discussed is FEN1; the disease is neoplasm.