In addition, a mutation in ATP13A2 was shown to cause α-synuclein accumulation and silencing of α-synuclein was able to attenuate the neurotoxicity induced by ATP13A2 depletion [177], suggesting that loss of ATP13A2 may contribute to PD pathology via α-synuclein accumulation. This evidence concerns the gene ATP13A2 and Parkinson disease.