It is likely that extracellular glutamate levels in brain are dysregulated in SLC25A22 deficiency patients [143] because it was shown that (i) reduced expression of SLC25A22 in glial cells leads to intracellular glutamate accumulation [148], and (ii) aberrant glutamate catabolism in astrocytes is associated with altered clearance of extracellular (synaptic) glutamate and early epileptic encephalopathy [149]. The gene discussed is SLC25A22; the disease is Epileptic encephalopathy.