Similarly, loss-of-function mutations in SLC39A14 have been reported in patients with high blood levels of Mn and accumulation of Mn in the brain (but not in the liver) and with juvenile-onset dystonia-parkinsonism (35), and Slc39a14-deficient mice again model these human phenotypes (36, 37). This evidence concerns the gene SLC39A14 and Parkinsonism.