Loss of function mutations of ATP13A2 are linked to multiple neurodegenerative conditions including Kufor-Rakeb Syndrome (KRS; PARK9), an autosomal recessive form of Parkinson’s disease (PD), early onset PD, Neuronal Ceroid Lipofuscinosis (NCL), complicated hereditary spastic paraplegia, and neurodegeneration with brain iron accumulation [3,4,5,6]. This evidence concerns the gene ATP13A2 and infantile neuronal ceroid lipofuscinosis.