Transcription in the vicinity of DNA double-strand breaks (DSBs) is suppressed via a process involving ataxia telangiectasia mutated protein (ATM) and H2AK119 ubiquitylation.(1) We discuss recent findings that components of the Polybromo and Brahma-related gene 1 (BRG1)-associated factor (PBAF) remodeling complex and the polycomb repressive complex (PRC1/2) are also required.(2) Failure to activate transcriptional suppression impedes a rapid DSB repair process.