Particularly, the activity of glutamine synthetase (GS) and the protein expression of system N glutamine transporter 1 (SN1), which are the key factors involved in the glutamate-glutamine cycle, were significantly upregulated, and inhibition of GLT-1 uptake activity by dihydrokainic acid, an inhibitor of GLT-1, blocked CEF-induced improvement in cognitive deficits, GS activity, and SN1 expression (Fan et al., 2018). The gene discussed is GLUL; the disease is Cognitive impairment.