This may contribute to the persistence of the higher number of γ-H2AX and 53BP1 foci at longer times from IR in APL cells (when compared with myeloid progenitors expressing normal PML protein and PML-NBs), resembling the deficiency in the repair of specific subset of DSBs described in DDR-defective cells.43 As PML-NBs are defined as baskets that contain proteins involved in the DSBS response, their disruption may cause a pan-nuclear dispersion of DDR proteins and consequently a defect in the DSBS tethering.10, 11, 13, 15, 16, 44. This evidence concerns the gene TP53BP1 and acute promyelocytic leukemia.