and references, see accompanying review by [Mark et al., 2009]). This could be because RA has critical functions in the transition region between the posterior 'stem' zone and the differentiating tissues, where Rarb and Rarg (as well as Rara) would be coexpressed. The posterior (tail bud) region needs to be actively protected from RA signaling by the action of the CYP26A1 enzyme [Abu-Abed et al., 2001; Sakai et al., 2001], and interestingly, the caudal defects occuring in Cyp26a1-null mutant mice are prevented by a compound inactivation of Rarg [Abu-Abed et al., 2003].