SLC13A5 and genetic developmental and epileptic encephalopathy: Along these lines, one aspect needs to be considered: while loss-of-function mutations in Drosophila or deletion of Slc13a5 in mice may convey survival and metabolic benefits [2,6], SLC13A5 deficiency in humans results in a recessive neurological disorder known as early infantile epileptic encephalopathy-25 (EIEE-25) [16,17].