37 Dysfunction of this pathway has been implicated in multiple aspects of PD pathogenesis, such as the reduced degradation, increased aggregation, and missorting of α-synuclein.38 Additionally, defects in synaptic vesicle endocytosis can disrupt the precise temporal coupling of exocytosis and endocytosis required for sustained neurotransmission, potentially contributing to synaptic dysfunction and neuronal loss in PD.39 Given its role as a scaffold protein, ITSN1 haploinsufficiency may exacerbate these processes by destabilizing endocytic protein networks and impairing vesicle recycling. This evidence concerns the gene SNCA and Parkinson disease.