Patients with classical type also have cognitive impairment.[3] They may also have symptoms suggesting impairment of pyramidal system, extrapyramidal system, and cerebellum.[9] The patients suffered from nonclassical Glut1-DS usually presents paroxysmal ataxia, weakness, and dyskinesia with or without epilepsy.[8] The discovery of SLC2A1 gene mutation is the most important diagnostic basis for Glut1-DS and provides specific therapy for this disease. This evidence concerns the gene SLC2A1 and drug-induced dyskinesia.