PARP inhibition has been demonstrated in numerous studies to provide benefit in a variety of neurodegenerative disease models in mice, from α-synuclein fibril injections,20 to TDP-43 toxicity,41 and models of Huntington’s disease.42 Kam et al.20 offered a compelling mechanism whereby endogenous PAR polymer accelerates aggregation to facilitate the formation of aggregates with enhanced neurotoxicity. The gene discussed is PARP1; the disease is neurodegenerative disease.