The most common genetic causes of ALS are the hexanucleotide repeat expansion (HRE) in the chromosome 9 open reading frame 72 (C9ORF72) gene1,2 and mutations in superoxide dismutase 1 (SOD1)3 TAR DNA-binding protein 43 (TARDBP)4 or fused in sarcoma (FUS).5,6 Several biological and cellular pathways are implicated in the onset and progression of ALS, leading to pathophysiological heterogeneity. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.