This, in turn, mitigates the accumulation of DNA lesion and averts hyperactivation of PARPs, which otherwise leads to further NAD+ depletion, precipitating cellular demise through various apoptotic pathways.31 Here, we demonstrate that inhibiting ACMSD elevates liver NAD+ content and diminishes DNA damage levels, thereby normalizing PARP1/2-induced PARylation and protecting livers of WD/TN mice. This evidence concerns the gene ACMSD and Wilson disease.