Although our findings are consistent with the general idea of a perturbation of AMPAR subunit expression as a feature of ALS pathology, cytoplasmic SFPQ aggregates may not cause an increase in the expression of GluA2-lacking Ca2+-permeable AMPARs, at least in cortical neurons, that are thought to mediate the excessive Ca2+ influx and death of motor neurons [40,50,51]. Here, GRIA2 is linked to amyotrophic lateral sclerosis.