Interestingly, genetic defects in lysosomal storage, such as variants of glucocerebrosidase associated with Gaucher disease [26], and defects in mitochondrial DNA synthesis, including mutations in POLG1[27,28], independently contribute to forms of parkinsonism, suggesting that impairments in lysosomal and mitochondrial homeostasis underlie certain shared pathways of neurodegeneration. This evidence concerns the gene GBA1 and Gaucher disease.