Similarly, depletion of kinesin-binding protein, KBP, which inhibits KIF1A activity, leads to the abnormal accumulation of both KIF1A and vesicles at neurite terminals (Kevenaar et al., 2016), and nonsense mutations of KBP cause Shprintzen-Goldberg syndrome (also called marfanoid-craniosynostosis syndrome), which is characterized by intellectual disability, skeletal abnormalities, and axonal neuropathy (Dafsari et al., 2015; Valence et al., 2013). This evidence concerns the gene KIF1A and Shprintzen-Goldberg syndrome.