Efforts to elucidate the mechanisms behind GBA1-associated PD have highlighted shared pathways in idiopathic PD including the loss and gain-of-function hypotheses, endoplasmic reticulum stress, lipid metabolism, neuroinflammation, mitochondrial dysfunction and altered autophagy–lysosomal pathway responsible for degradation of aggregated and misfolded a-synuclein. The gene discussed is GBA1; the disease is Parkinson disease.