Riboflavin (vitamin B2) is the solitary precursor for the biologically active cofactors known as the flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) molecules [1]. These cofactors are required in oxidation-reduction (redox) reactions and act as cofactors for the electron transfer flavoprotein (ETF) and its dehydrogenase (ETFDH) [2]. The ETF and ETF-DH form electron transport pathways for at least 12 mitochondrial flavoprotein dehydrogenases involved in amino acid, fatty acid, and choline metabolism [3]. Variations of the ETF or ETF-DH cause multiple acyl-CoA dehydrogenation deficiencies (MADDs), and riboflavin metabolism or transport genetic defects can also cause MADD or varying degrees of progressive neurodegenerative diseases such as riboflavin transporter deficiency (RTD) [3]. There are three human riboflavin transporter (RFVT) homologs: RFVT 1 to 3, encoded by genes SLC52A1 to SLC52A3, respectively [4]. RFVTs are widely distributed in the body and SLC52A1 is highly expressed in the placenta and intestine [3]. SLC52A2 is rather ubiquitously expressed, mainly in the brain, and, although SLC52A3 is most highly expressed in the testes, which also expressed in the intestine and prostate [3]. There are three types of RTDs and these

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