Cilia are microtubule-based organelles that extend from the surface of various types of cells in vertebrates. Cilia are maintained by intraflagellar transport (IFT) and play important roles in sensing and moving across species. At the distal tip of the cilia/flagella, IFT complexes turn around to switch from anterograde to retrograde transport, however, the underlying regulatory mechanism is unclear. Here, we identified Intestinal Cell Kinase (ICK) localization at the tip of cilia as a regulator of ciliary transport. We generated and analyzed retina- or brain-specific ICK-deficient mutant mice as well as conventional ICK-deficient mutant mice. These mice showed phenotypes defective in Hedgehog (Hh) signal transduction in multiple organs. We found that ICK-deficient cells formed cilia with mislocalized Hedgehog signaling components. Unexpectedly, we found that ICK is required for ciliogenesis in neural progenitor cells but not in mature neurons. Loss of ICK caused the accumulation of IFT-A, IFT-B, and BBSome components at the ciliary tips. In contrast, overexpression of ICK induced the strong accumulation of IFT-B but not IFT-A or BBSome components at ciliary tips. In addition, ICK directly phosphorylated Kif3a, while inhibition of this Kif3a phosphorylation affected ciliary formation. Our results suggest that ICK is a Kif3a kinase and essential for proper ciliogenesis in development by regulating ciliary transport at the tip of cilia.