Griffith et al. (2016) reported that Kir6.2 subunits were significantly increased in reactive astrocytes in both patients with AD and the hippocampus in 3 × Tg-AD mice. Since excitatory amino acid transporter 2 is reduced in AD in order to promote glutamate uptake by K-ATP channels in astrocytes, the upregulation of Kir6.2 in AD may be a compensatory effect on its glutamate uptake (Griffith et al., 2016). This evidence concerns the gene SLC1A2 and Alzheimer disease.