The presynaptic neuronal protein, α-synuclein, has long been associated with PD.71 More recently, the activation of PARP1 was shown to exacerbate α-synuclein toxicity.56 Further, preformed fibrils of recombinant α-synuclein induced PARP1 activation, resulting in α-synuclein aggregates and cell death via parthanatos, a non-apoptotic mechanism involving PAR and apoptosis-inducing factor (AIF).72 The use of PARP inhibitors was able to rescue toxicity induced by the α-synuclein preformed fibrils. The gene discussed is PARP1; the disease is Parkinson disease.