In contrast to a previous report suggesting that knockdown of RAD51 can fully restore fork degradation in the absence of CTIP [43], we found that cells with RAD51 depleted displayed fork degradation to the same extent as when FEN1 is knocked down, and double depletion of FEN1 and RAD51 did not trigger fork degradation, suggesting that FEN1 and RAD51 are involved the same regulatory pathway and that they show functional variations in glioma cells under certain conditions (Fig. 3i). The gene discussed is RAD51; the disease is glioma.