Notably, treatment of mice with Cockayne syndrome with PARP1 inhibitors or NAD+ supplementation reversed inactivation of SIRT1 and mitochondrial defects, resulting in slowed ageing, extended lifespan and amelioration of severe phenotypes caused by PARP1 hyperactivation in response to extensive DNA damage and genotoxic stresses [50, 51]. Here, SIRT1 is linked to Cockayne syndrome.