Importantly, reduced transcriptional recovery following oxidative stress was also observed in patient-derived human fibroblasts with XRCC1 mutations as well as Xrcc1Nes-cre mouse cerebellar neurones, and these defects were again prevented by PARPi, implicating PARP1-induced transcriptional repression in neurological disease (Fig. 3 and Extended Data Fig. 4). This evidence concerns the gene XRCC1 and nervous system disorder.