Our results indicate that excess Vegfa is associated with the pathological skeletal phenotype in human CYP26B1 deficiency and in rats with hypervitaminosis A. There is also a strong resemblance between the rat hypervitaminosis A bone phenotype and secondary manifestations seen in bones of patients with myelofibrotic disorders, findings which further support previous studies showing a powerful effect of vitamin A on bone tissue and suggest that an early part of the mechanism is mediated by excess Vegfa and disturbed bone marrow microvessel integrity. The gene discussed is CYP26B1; the disease is hypervitaminosis A.