Intriguingly, the neurological consequences of conditional Xrcc1 deletion in mouse, which include cerebellar ataxia, seizures and shortened life-span, are in part the result of Parp1 hyperactivation15,16, highlighting the likely pathological consequences of aberrant and/or excessive PARP signalling at unrepaired SSBs. Here, PARP1 is linked to aceruloplasminemia.