Although glutamate neurotoxicity is widely endorsed by the scientific community as one of the main mechanisms in the ALS pathophysiology (Vucic et al., 2014) and REST is an important transcription factor regulating several glutamate receptor subunits (Rodenas-Ruano et al., 2012), our in vitro model could not be used to evaluate glutamate neurotoxicity, since it has been demonstrated that, even if differentiated, NSC34 cells do not express glutamate receptors (Madji Hounoum et al., 2016). Here, REST is linked to amyotrophic lateral sclerosis.