Genetic studies further support a mechanistic link between LD biology and PD pathogenesis: GBA mutations promote to glucosylceramide accumulation and upregulate PLIN2 in iPSC-derived dopaminergic neurons (Russo and Riessland, 2024), LRRK2 mutations alter phospholipid metabolism relevant to LD monolayer composition (Galper et al., 2022), and SMPD1 mutations impair lysosomal lipid degradation, resulting in secondary LD accumulation (Alecu and Bennett, 2019; Fais et al., 2021). The gene discussed is GBA1; the disease is Parkinson disease.