Collectively, our findings demonstrate that primary cilium anomalies occur more predominantly in the RAB23 loss-of-function neuronal cell types (albeit in distinct neuronal populations) and this phenomenon is consistently observed in the zebrafish morphants, transgenic KO mice, and human disease models of Carpenter syndrome patients, suggesting that the function of RAB23 in the primary cilium is context-dependent and evolutionarily conserved. The gene discussed is RAB23; the disease is Carpenter syndrome.