IFT52 is a core component of the intraflagellar transport (IFT)-B complex essential for ciliogenesis and ciliary function 1. It mediates bidirectional cargo transport along the ciliary axoneme by stabilizing the interaction between IFT-B1 and IFT-B2 subcomplexes and facilitating binding to kinesin-II motors 2. IFT52 is required for anterograde transport of ciliary proteins including IFT88, ensuring proper cilia assembly, maintenance, and length regulation 1. Beyond its canonical ciliary role, IFT52 regulates microtubule dynamics and centrosome cohesion through interactions with centrin at centrioles 3. Pathogenic variants disrupt IFT-B complex assembly and reduce ciliary IFT-B levels, impairing localization of cargo proteins like ICK/CILK1 and KIF17 to ciliary tips 2. IFT52 mutations cause short-rib thoracic dysplasia 16 with or without polydactyly (SRTD16), a skeletal ciliopathy characterized by thoracic and limb abnormalities 3. IFT52 variants are also associated with retinal degeneration and Leber congenital amaurosis through disruption of photoreceptor ciliary function 4. Phenotype severity correlates with mutation type: missense mutations impair complex assembly and cilia length, while nonsense mutations produce partially functional proteins 3. IFT52 dysfunction affects osteogenic differentiation and sensory neuronal development, highlighting its importance in skeletal and sensory system development 5.