This is, of course, also implied by the reduced GluA2 Q/R site editing efficiency in several neurological conditions including Alzheimer’s disease [29–31], schizophrenia [30], Huntington’s disease [30], amyotrophic lateral sclerosis [32], astrocytoma [33], stroke [34] and cocaine seeking behaviour in rats [35] and by prior observations that overexpression of ADAR2, or overexpression of edited GluA2, can provide therapeutic benefit in some models [34, 35, 84]. Here, GRIA2 is linked to juvenile Huntington disease.