Furthermore, in mouse and human, cleft palate phenotypes may arise as a consequence of mutations in Wnt3 and Wnt9b (Niemann et al., 2004; Juriloff et al., 2006), and perturbation of Wnt/β-catenin signaling has been implicated in CATSHL syndrome, a human developmental disorder involving craniofacial bone malformation and mispatterning of the pharyngeal arches (Sun et al., 2020). Here, WNT3 is linked to Camptodactyly - tall stature - scoliosis - hearing loss.