We then used genetic and pharmacological approaches to manipulate catB expression and function in cell lines and induced pluripotent stem cell-derived dopaminergic neurons and assessed lysosomal activity and the handling of aggregated synuclein fibrils.<h4>Results</h4>We first identified specific non-coding variants in <i>CTSB</i> that drive the association with PD and are linked to changes in brain <i>CTSB</i> expression levels. This evidence concerns the gene TYRP1 and Parkinson disease.