Recently, we demonstrated using an Xrcc1‐defective mouse model (Xrcc1Nes‐Cre) that SSBR‐defective cerebellum possesses elevated steady‐state levels of poly(ADP‐ribose) resulting from the hyperactivation of Parp1, leading to the loss of cerebellar interneurons and cerebellar ataxia (Lee et al,2009; Hoch et al,2017). Here, PARP1 is linked to aceruloplasminemia.