In the subsequent part of this study we analyzed normal human endothelial and osteoblast cells treated with RA and rats with hypervitaminosis A to further corroborate the similarities between CYP26B1 insufficiency and hypervitaminosis A. These analyses also added evidence that Vegfa and microvascular damage appears as early contributors to the hypervitaminosis A bone pathology. The gene discussed is CYP26B1; the disease is hypervitaminosis A.