Mutations in SLC25A12 are responsible for a disease characterized by developmental delay, epilepsy, hypotonia, hypomyelinization and decreased N-acetylaspartate in brain [16,17], whereas mutations in SLC25A13 result in type II citrullinemia, which manifests with a dislike for carbohydrates, the inability to consume alcohol, citrullinemia and hyperammonemia leading to encephalopathy and neuropsyachiatric symptoms [18,19,20]. Here, SLC25A13 is linked to citrullinemia type II.