Specifically, the Huntington’s disease-related Huntingtin protein, which undergoes polyQ expansion in the disease6 (HTT-polyQ), aggregates through a process of oligomerization and fibril formation7,8, while many ALS-related proteins, including TDP-43 and FUS, form aggregates in a process of aberrant liquid-liquid phase separation9,10. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.