The Hippo pathway effector proteins YAP1 (Yes-Associated Protein 1) and TAZ (Transcriptional coActivator with PDZ-binding motif) are key regulators of a range of developmental processes in many developing tissues. Haploinsufficiency of the transcriptional co-regulator YAP1 in humans can lead to a rare congenital condition presenting with eye and craniofacial phenotypes, including cleft palate and/or lip (1). The developmental and molecular mechanisms underlying the cleft palate/lip phenotypes are unknown. We investigated the pathogenesis of the craniofacial abnormalities associated with the human disorder by deleting both Yap and Taz in the developing cartilage, a primary component of craniofacial structures, of mice. Yap/Taz chondrocyte-specific conditional knockout (cKO) animals present with a range of palate defects and we investigated the morphogenesis and molecular changes underlying these defects, including changes in the expression of important cartilage extracellular matrix components, such as Aggrecan and collagens, in the developing face. Altogether, our work suggests that loss of YAP1 specifically in the cartilage component of the developing craniofacial structures contributes to the cleft palate phenotype observed in human YAP1 haploinsufficiency disease.