In our previous report (27), we also demonstrated that the polβ/XRCC1 complex enhances the handoff of nicked repair products to the final ligation step and XRCC1 cancer-associated (P161L, R194W, R280H, R399Q, Y576S) and cerebellar ataxia–related (K431N) variants impact this channeling process distinctly depending on the nature of the mutation. This evidence concerns the gene XRCC1 and aceruloplasminemia.