Furthermore, we observed that interruption of HKDC1 by shHKDC1 significantly suppressed in vivo tumor formation and increased mouse survival; overexpression of SOD2 completely, whereas OGG1 only partly, reversed this effect, suggesting that the HKDC1 interruption-mediated antitumor effect was due to the generation of ROS and subsequent ROS-mediated DNA damage. Here, HKDC1 is linked to neoplasm.