The lack of unedited GluA2 in iPSC-derived motor neurons from sporadic ALS or familial ALS patients carrying FUSH517D mutations [113,114] may be due to either or both of the following reasons: the considerably shorter life time of iPSC-derived differentiated motor neurons in culture than that of the degenerating motor neurons in ALS patients or the large difference in the cellular environment between the in vitro culture condition and the in vivo microenvironmental conditions surrounding the degenerating motor neurons in patients. Here, GRIA2 is linked to amyotrophic lateral sclerosis.