Finally, RNAi-mediated knockdown of endogenous ATP13A2 in vitro (a lysosomal P-type ATPase associated with familial PD) or expression of PD-associated mutations of ATP13A2 promote modest mitochondrial fragmentation, lead to impaired mitochondrial flux, and cause an aberrant accumulation of dysfunctional mitochondria, and concomitant impaired biogenesis [55,56]. The gene discussed is ATP13A2; the disease is Parkinson disease.