The importance of a preserved GMAP/IFT20 complex for a milder cellular and clinical phenotype of ODCD was strongly supported by a third essential difference to ACG1A detected in patient-derived cells: whereas a strong reduction of total membrane trafficking was observed in ACG1A, the global secretory capacity of the Golgi was normal in ODCD, at least in primary fibroblasts. This evidence concerns the gene GAL and odontochondrodysplasia 1.