Our results that α-synuclein levels accumulate in the midbrain of GBA+/L444P mice (Fig. 1) is consistent with previous findings in Gaucher’s disease animal models [50] and support the hypothesis that GBA mutations might disrupt cellular pathways related to lysosomal degradation of α-synuclein and the subsequent accumulation of α-synuclein [51]. The gene discussed is GBA1; the disease is Gaucher disease.