By contrast, Cilk1-deficient cells exhibit excessive accumulation of Smo within the primary cilium even under unstimulated conditions, without corresponding activation of Hedgehog signaling.34 While loss-of-function mutations in primary cilia-related genes such as Ift88, Ofd1, and Kif3a cause severe developmental defects, including cleft palate and abnormal tooth patterning,37–39 the specific impact of Cilk1 on tooth development remains unclear. This evidence concerns the gene IFT88 and cleft palate.