The variant is probably associated with a decreased level of EAAT2 protein, elevated glutamate level in plasma and synapses, and with a higher frequency of early neurological worsening in stroke of the variant patients [22], indicating that LRRFIP1/GCF2 represses the expression of EAAT2 in the variant, and then the elevated glutamate contributes to excitotoxity after a stroke. The gene discussed is SLC1A2; the disease is stroke disorder.