Further, the loss of VMAT2 was found to be a key pathogenic event in a non-human primate model of PD [11] and, in congruence, reduced VMAT2 expression lead to a stronger phenotype in rodents in a neurotoxin induced PD model [12] whereas VMAT2 overexpression was protective [13,14]. Here, SLC18A2 is linked to Parkinson disease.