AbstractParkinson's disease (PD) is a neurodegenerative disease that is common in middle‐aged and elderly people, and its onset is related to multiple factors, such as heredity, environment, and age. The vesicle protein sorting 35 (VPS35) gene was found to be a late‐onset autosomal dominant familial PD (PARK17) causative gene. The protein encoded by this gene is located in the endosome and aggregates with other membrane proteins to form a retromer complex, which participates in the membrane protein cycle between the endosome and the Golgi network. Increasing evidence shows that VPS35 may participate in the pathogenesis of PD by affecting autophagy, mitochondria, neurosynaptic transmission, dopamine signaling pathways, and so forth, and it can interact with other disease‐causing genes of familial PD. This article aimed to review the functions of VPS35 and the mechanism of its mutations in PD that have been discovered in recent years.