In another example, genome-wide expression analysis of motor neurons (the neuronal subtype predominantly affected in amyotrophic lateral sclerosis (ALS)) derived from ZFN-corrected SOD1 mutant hiPSCs revealed a unique, disease-dependent transcriptional signature indicative of increased oxidative stress, reduced mitochondrial function, altered subcellular transport, and activation of the ER stress [148]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.