On the vitamin A deficiency-susceptible Rbp4−/− background, Bco1−/−Rbp4−/− female mice generated severely malformed Bco1+/−Rbp4−/− embryos (carrying one copy of the wild-type Bco1 allele), whereas β-carotene supplementation rescued 61% of these offspring from developmental defects, since the embryos could cleave β-carotene via BCO111. The gene discussed is BCO1; the disease is vitamin A deficiency.