Structure–function analyses have shown that the G‐rich domain (amino acids 156–262) and C‐terminal domain (amino acids 450–526) of FUS are required for interaction of FUS and histone deacetylase 1 (HDAC1) (Shang & Huang, 2016), which harbor most of the ALS mutations (Figure 3c). This evidence concerns the gene FUS and amyotrophic lateral sclerosis.