The increased SIRT1–KU70 interaction can favor DNA repair by opening the chromatin, and this interaction can increase the likelihood of BCR-ABL mutations in chronic myeloid leukemia (CML) [88,89], and has been involved in resistance to treatment with tyrosine kinase inhibitors [90,91]. Here, XRCC6 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.