Kif7, a component of the kinesin complex for anterograde intraflagellar transport in cilia, is a key regulator in the Hedgehog (Hh) signaling pathway [1,2,4,7]. The Hh pathway is highly conserved and crucial for embryonic development, with Kif7 involved in the signaling cascade that impacts the balance between activator and repressor forms of Gli transcription factors [2].

Mutations in Kif7 have been linked to various disorders. In humans, these include hydrolethalis, acrocallosal syndrome, Joubert syndrome, and intellectual disability with isolated dysgenesis of corpus callosum [1,5,7]. In zebrafish, kif7 mutants display severe scoliosis, suggesting a role in this spinal disorder [6]. In prostate cancer, KIF7 is downregulated, and its coiled-coil domain can attenuate tumor growth through LKB1-mediated AKT inhibition [3].

In conclusion, Kif7 is essential for normal development and its proper function in the Hh signaling pathway. Dysfunction due to mutations can lead to a range of developmental disorders and potentially cancer. The study of Kif7 through genetic models like zebrafish mutants and in cancer cell-derived xenografts helps in understanding its role in disease pathogenesis, providing insights for potential therapeutic strategies.