The majority of ALS is sporadic with unknown etiology (90-95%); however, the remaining cases are familial (fALS) and have been linked to genetic mutations in genes such as Cu2+/Zn2+ superoxide dismutase (SOD1), Alsin (Als2), dynactin, angiogenin, senataxin, vesicle-associated membrane protein/synaptobrevin-associated membrane protein B, TAR DNA binding protein 43 (TDP43), fused in sarcoma (FUS), optineurin, and ubiquilin 2, or a hexanucleotide repeat expansion in C9ORF72[5-18]. Here, TARDBP is linked to amyotrophic lateral sclerosis.