Other PD-associated gene variants such as TMEM175, Parkin (PRKN) and LRRK2 have also been shown to cause a reduction in CTSB levels and enzymatic activity in cellular and mouse models [36–38], implying that the deficiency in CTSB lysosomal function is a contributing factor to PD pathology. This evidence concerns the gene PRKN and Parkinson disease.