BUB1B and neoplasm: In addition to those canonical functions, the results from the current study suggest that a constitutive upregulation of BUB1B/BUBR1 throughout the cell-cycle phases in CRT-recurrent tumor offers a redundant function to repair DSBs, which dominantly exploits mutagenic NHEJ rather than precise NHEJ or HR, leading to the CRT-resistant clones harboring accumulated mutations.