In the complete absence of RBP4, from the work of Quadro and colleagues in 1999, it was found that normal visual development and function can be sustained with sufficient vitamin A intake in mice from alternate pathways of retinoid transport, but disease phenotypes were observed in RBP4 null mice in times of vitamin A deficiency likely due to the lack of hepatic mobilization of retinoids in storage [26]. Here, RBP4 is linked to vitamin A deficiency.