While ATP13A2 knockout from primary neurons and ATP13A2 PD patients-derived fibroblasts lead to lysosomal dysfunction with subsequent accumulation of α-synuclein and toxicity [115, 121], ATP13A2 knockout mice had lysosomal dysfunction and toxicity without the accumulation of α-synuclein [120]. The gene discussed is ATP13A2; the disease is Parkinson disease.