For instance, it is clear that complete absence of EAAT2 results in spontaneous epilepsy (Tanaka et al. 1997) and increased extracellular glutamate (Mitani and Tanaka 2003; Takasaki et al. 2008), but studies of humans with epilepsy have not uncovered any direct link to glutamate transporter expression (Tessler et al. 1999; Akbar et al. 1997; Bjørnsen et al. 2007). The gene discussed is SLC1A2; the disease is epilepsy.