Intriguingly, we also detected increased PARP1 trapping in primary human fibroblasts from XRCC1-mutated disease, and we reported recently that loss of cerebellar interneurons and cerebellar ataxia in Xrcc1-deleted mice are suppressed greatly by Parp1 deletion (Hoch et al., 2017). This evidence concerns the gene XRCC1 and cerebellar ataxia.