Overall, these data indicate that the trafficking and maturation defects of CTSD, CTSB, and CTSL in midbrain neurons harbouring synucleinopathies (A53T SNCA mutation and SNCA gene triplication), could be rescued by enhancing hydrolase transport towards the lysosomes via activation of the ykt6 pathway, using the small compound FTI. The gene discussed is YKT6; the disease is synucleinopathy.