While it remains unclear exactly how ATP13A2 dysfunction leads to neurodegeneration, early in vitro studies in yeast, dopaminergic cells, and iPSCs show ATP13A2 dysfunction impacts lysosomal and mitochondrial function and when overexpressed can protect against alpha-synuclein (αSyn), a key protein in PD, and heavy metal toxicity [14,15,16,17]. This evidence concerns the gene ATP13A2 and Parkinson disease.