Lee and colleagues have demonstrated that ARSA, despite being a lysosomal protein, directly interacts with α-synuclein present in the cytosol of the cell, acting like a molecular chaperone: some ARSA disease-causing variants are responsible for a reduction of this interaction and a consequent α-synuclein aggregation, whereas other variants, known to be protective against parkinsonism, encode for proteins that have a stronger interaction with cytoplasmatic α-synuclein [127]. The gene discussed is ARSA; the disease is Parkinsonism.