Taking these observations together, we hypothesized that (1) ALS/FTD mutations in the FUS LC domain (e.g., S96del and G156E) might directly increase the propensity of the LC domain to induce FUS assembly into higher order structures; while (2) ALS/FTD mutants in the C terminus would indirectly have the same effect by reducing the anti-aggregation effect of the C terminus (Figure S4). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.