Furthermore, normalization of Ca2+ influx through the AMPA receptors, including expression of Q/R site-edited GluA2 in the absence of ADAR2 or delivery of the human ADAR2 gene for normalizing RNA editing at the GluA2 Q/R site19, 21, effectively rescued the ALS phenotype and death of motor neurons associated with the TDP-43 mislocalization in the AR2 mice19, 20. Here, TARDBP is linked to amyotrophic lateral sclerosis.