The resulting bi-allelic epileptic encephalopathy is known as SLC13A5 deficiency disorder (SDD) and may also be referred to as developmental epileptic encephalopathy-25, early infantile epileptic encephalopathy-25, SLC13A5 epilepsy, SLC13A5 Citrate Transporter Disorder, Citrate Transport Disorder, SLC13A5 Deficiency, or Kohlschutter-Tonz Syndrome (non-ROGDI) [4,5,8,9]. This evidence concerns the gene SLC13A5 and Amelo-cerebro-hypohidrotic syndrome.