The hyperexcitability observed in ALS patients through clinical neurophysiological studies is successfully recapitulated in motor neurons derived from iPSCs of ALS patients with superoxide dismutase 1 (SOD1) and chromosome 9 open reading frame 72 protein (C9orf72) mutations; this hyperexcitability was lost in motor neurons generated from genetically corrected iPSC lines [224]. Here, C9orf72 is linked to amyotrophic lateral sclerosis.