Interestingly, the genetic inactivation of Parp1 (poly (ADP) ribose polymerase 1) rescued ADP ribose levels and reduced the loss of cerebellar neurons and ataxia in Xrcc1-defective mice, implying that PARP1 hyperactivation was neurotoxic to cerebellar neurons [263]. Here, XRCC1 is linked to cerebellar ataxia.