A recent study showed that treatment with a glucosylceramide synthase inhibitor miglustat to reduce glycosphingolipid accumulation and overexpression of GBA1 to augment GBA1 activity can reverse the GBA1 deficiency-induced destabilization of α-synuclein tetramers and related multimers and protect against the α-synuclein preformed fibril-induced toxicity in hDA neurons derived from GBA + PD iPSCs, which suggest therapeutic opportunities for GD and PD patients [91]. Here, UGCG is linked to Parkinson disease.