The hypothesis that ATG9A mislocalization is a key mechanism in the pathogenesis of AP-4-HSP is supported by the independent work of the Robinson12, Kittler14 and Bonifacino11,13,60 groups, in addition to our own work15,21,24,25, and by the overlapping phenotypes of AP-413,14,26 and Atg9a28 knockout mice. The gene discussed is ATG9A; the disease is hereditary spastic paraplegia.