In support of this hypothesis, it has been shown previously that genetic targeting of vitamin A metabolizing enzymes or transport proteins (Bco2, Bco1, Lrat, Rpe65, Rbp4 or Stra6) in zebrafish provokes a loss of ocular retinoid availability and subsequent signaling during early eye development that results in microphthalmia and retinal phenotypes at larval stages [31,33,57,58,60,61]. Here, BCO1 is linked to microphthalmia.