Postmortem brain tissue analyses, patient-derived IPS-cell models, and CSF studies show decreased levels of GCase activity paralleled by alpha-synuclein accumulation in wild-type PD patients and in PD patients with mutations in LRRK2, parkin, and DJ-1. Interestingly, LRRK2 kinase activity seems to regulate GCase activity in an inverse pattern (Parnetti et al., 2017; Burbulla et al., 2019; Ysselstein et al., 2019). This evidence concerns the gene PRKN and Parkinson disease.