Analogous, overexpressing GBA p.Leu444Pro in SHSY-5Y neuroblastoma cells and knock-in of heterozygous GBA p.Leu444Pro in mice both trigger mitochondrial dysfunction by inhibiting autophagy and mitochondrial priming, a process by which autophagy receptor proteins are recruited to damaged mitochondria for degradation [196]. Here, GBA1 is linked to neuroblastoma.