Mice defective for either Gria2 mRNA expression or its editing exhibit detrimental phenotypes in synaptic function, development, and behavior (Isaac et al, 2007) and disruption of Gria2 function is associated with neurological disorders such as cerebral ischemia, amyotrophic lateral sclerosis, pain, and epilepsy (Cull-Candy et al, 2006). The gene discussed is GRIA2; the disease is amyotrophic lateral sclerosis.