These case reports show that RFVT 1 is essential for placental transport of riboflavin, and that impaired riboflavin transport due to RFVT1 haploinsufficiency can result in an MADD-like clinical and biochemical phenotype of the newborn, even if the newborn himself does not carry the SLC52A1 variant. This evidence concerns the gene SLC52A1 and multiple acyl-CoA dehydrogenase deficiency.