In addition, we show DYNLL1-53BP1 interplay plays an essential role in mediating toxic NHEJ events in Brca1 mutant cancer cells: deletion of DYNLL1 or its transcriptional regulator ATM substrate Chk2-interacting Zn2+ finger protein (ASCIZ; also known as ATMIN/ZNF822) is strongly selected for in BRCA1-deficient tumour cells, and results in PARPi resistance in vitro and in vivo. This evidence concerns the gene TP53BP1 and neoplasm.