CYP26B1 and hypervitaminosis A: First, we show that CYP26B1 insufficiency induces local pathological accumulation of bone resorbing osteoclasts in the periosteum, similar to that consistently observed in hypervitaminosis A. This observation, together with our recent finding that calvarial hypoplasia previously described in CYP26B1 insufficiency (Laue et al., 2011) is also characteristic of hypervitaminosis A in mice (Lind et al., 2017), add support to the notion that the skeletal defects observed in the human homozygous for a CYP26B1 mutation are caused by aberrant RA levels.