Indeed, retention of FUS in the cytoplasm, followed by its accumulation in cytoplasmic inclusion, is a well-recognized pathological feature of ALS.53 However, as for TDP-43, there is a continuous debate around the contribution of the associated reduction in nuclear expression or cytoplasmic gain of toxic function to motor neuron death in ALS pathogenesis. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.