IFT57 is an essential intraflagellar transport protein required for primary cilium formation and maintenance 1. As a component of IFT complex B, IFT57 facilitates anterograde transport of cargo proteins from the ciliary base to the tip 2. IFT57 regulates kinesin II dissociation from IFT particles, enabling efficient ciliary protein transport 1. Beyond ciliogenesis, IFT57 participates in sonic hedgehog signaling, which depends on intact primary cilia 3, and localizes G protein-coupled receptors including dopamine receptor DRD1 to cilia 4. IFT57 possesses pro-apoptotic functions through interaction with HIP1, recruiting caspase-8 5. Mutations in IFT57 cause ciliopathies, including orofaciodigital syndrome with skeletal dysplasia 3 and Bardet-Biedl syndrome characterized by retinal degeneration, polydactyly, and obesity 2. IFT57 disruption also impairs TRAF7-mediated cilia maintenance, contributing to meningiomas and congenital heart defects 6. Emerging evidence suggests IFT57 dysregulation associates with neurodevelopmental conditions; altered IFT57 expression correlates with attention-deficit/hyperactivity disorder pathophysiology 7. Additionally, IFT57 coregulation with CD47 influences cancer survival outcomes across multiple tumor types 8.