Further, it has been shown to be essential for mouse development, with Slc52a3 deficiency resulting in early embryonic lethality associated with defects in placental formation, but dispensable for neural differentiation and short-term maintenance [190], suggesting that in BVVLS patients with mutations in RFVT3 alternative transporters may act during embryogenesis to allow full-term development. This evidence concerns the gene SLC52A3 and riboflavin transporter deficiency.