Stem cell modeling of ALS has shown that A4V mutation of SOD1 causes a proapoptotic phenotype, reduction in neurite outgrowth, and survival while E100G mutation leads to activation of endoplasmic reticulum stress pathway, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinases (JNK) signaling pathways (28, 29). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.