The future lines of research are: the improvement of the understanding of the biological mechanisms underlying neurodegeneration in AFD patients (deposition of Gb3 versus cerebrovascular lesions in the nigrostriatal network); the existence of a compensatory mechanism of increased a-GAL A activity upon PD neurodegeneration, as observed in LRRK2 carriers; the prospective multimodal comparison between AFD and sporadic PD patients; and finally the role of ERT chaperone therapy in neurodegeneration in AFD, remembering that ERT does not penetrate the blood–brain barrier. Here, LRRK2 is linked to Nager acrofacial dysostosis.