The most known mutations that produce the typical adult-onset ALS phenotype in the familial cases are related to the copper/zinc superoxide-dismutase-1 gene (SOD1 ), Tar DNA-binding protein gene (TARDBP ) (previously known as TDP-43), DNA/RNA-binding protein called FUS (fused in sarcoma), TLS (translocation in liposarcoma), and the most recent hexanucleotide repeat expansion in C9ORF72 [1,3]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.