The prion-like DNA/RNA-binding protein fused in sarcoma (FUS), whose mutation is associated with the motor neuron degenerative disease Amyotrophic Lateral Sclerosis (ALS) through the conversion of FUS-formed liquid droplets into solid aggregates in the neurons, was found to accumulate at DNA damage sites [58], where it mediated the retention of Ku autoantigen 80 (KU80) and the induction of high order of gamma histone H2A X variant (γH2AX) accumulation in a way dependent on the LLPS function of FUS [59]. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.