In our Subjects, the decreased RA catabolism and increased sensitivity to RA, as a consequence of CYP26B1 deletion could explain features similar to those noted by Laue et al. [16] (e.g. brachycephaly for both subjects, and for Subject 1, the delayed closure of the metopic suture) and in general compromise the craniofacial, skeletal development and neuronal functioning. This evidence concerns the gene CYP26B1 and Brachycephaly.