Mechanistically, it was reported that FUS mediates the recruitment of histone deacetylase 1, KU70, NBS1, and phosphorylated H2AX (γH2AX), and ATM at sites of DNA damage and that this recruitment pathway as well as FUS-dependent repair was compromised by ALS/FTD-associated mutations (27). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.