Experimental studies have shown that specific inhibition of GLT-1 expression in astrocytes significantly elevates extracellular glutamate concentration, leading to a significant increase in seizure frequency and duration in epilepsy model animals, and restoration of glutamate transporter function through enhancement of GLT-1 stability has become an important research direction in antiepileptic therapy (Chotibut et al., 2014; Shibata et al., 1997; Norris et al., 2025). The gene discussed is SLC1A2; the disease is epilepsy.