Consistent with this finding, sequencing of the 3′-untranslated region (3′-UTR) of FUS mRNA in ALS patients, with no mutations in the currently known ALS-associated genes, identified four mutations linked to a marked increase in the accumulation of FUS18, indicating that not only the nuclear–cytoplasmic imbalance of the mutant FUS, but also alterations in the physiological levels of the wild-type (wt) contribute to the pathogenesis of ALS. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.