RNF168 and breast cancer: Moreover, the phosphorylation levels of KDM1A were upregulated in breast cancer, UCEC, and LUAD, and the phosphorylation of KDM1A at S131 and S137 was experimentally supposed to play a role in regulating RNF168-dependent 53BP1 recruitment in response to DNA damage and resisting DNA damaging agents [23, 42].