Aiming to elucidate Rab23’s role in the functional integrity of the primary cilium and the consequence of its loss in the pathogenesis of Carpenter syndrome, we established mouse mutants of Rab23. In order to generate transgenic knockout mouse mutants of Rab23, Rab23f/f homozygous mice [18] were crossed with a β-actin-Cre driver line to induce global deletion of Rab23 in the progenies (herein named actin-CKO). This evidence concerns the gene ACTB and Carpenter syndrome.