Genetic models, targeting LRRK2 and GBA1, offer insights into PD risk factors; LRRK2 models affect mitochondrial function and autophagy (Tsika et al., 2014), while GBA1 models demonstrate glucocerebrosidase deficiency and moderate α-synuclein buildup, aiding the study of lysosomal dysfunction in PD pathology and therapies (Polinski et al., 2021). The gene discussed is GBA1; the disease is hyperinsulinemic hypoglycemia, familial, 4.