Both mRNA and protein levels of EAAT1 were reported to be increased, whereas EAAT2 mRNA and protein levels were decreased relative to controls in samples from the frontal cortex (BA10).142 As ∼90% of glutamate is removed from the synapse by EAAT2, Rao et al. hypothesize that their results remain largely consistent with the premise that BD is characterized by hyperglutamatergic signaling.142 Of note, riluzole, which increases the expression of EAAT2, has shown some efficacy in treatment-resistant depression and as adjunctive therapy for bipolar depression in mostly open-label studies.126, 143. The gene discussed is SLC1A2; the disease is bipolar disorder.