We found that, in contrast to the WT construct, neither of the cancer-associated mutant BAF180 constructs was able to fully rescue either the DSB repair defect or the failure to arrest transcription observed in the BAF180-depleted cells (Figures 6B and 6C), raising the possibility that the function of BAF180 in repressing transcription near DSBs contributes to its tumor suppressor activity. The gene discussed is PBRM1; the disease is neoplasm.