With regard to FABP5, the specific ligand for FABP5 abolishes α-synuclein accumulation and translocation to mitochondria, which alleviates neurotoxicity in Parkinson’s disease model neuronal cells [129], as well as ameliorates oligodendrocyte injury in multiple sclerosis mouse models [131] and psychosine-induced apoptosis in Krabbe disease models [130]. The gene discussed is FABP5; the disease is Krabbe disease.