The two most relevant genetic mutations associated with ALS are a defect in the hexanucleotide repeat expansion (HRE) in intron 1 of the C9orf72 gene (which makes a protein that regulates actin dynamics and endosomal recycling of GluR1 at the synapse) (148), and in the free radical scavenging enzyme Cu,Zn-superoxide dismutase (SOD1) gene (149). Here, SOD1 is linked to amyotrophic lateral sclerosis.