Based on this evidence that aggregates in the nucleus are less perturbing than their cytosolic counterparts, our results showing that MIF inhibits the sequestration of mutant SOD1 from the nucleus to the cytosol may provide an additional explanation for MIF’s protective effect especially considering the fact that nucleocytoplasmic transport defects play a central role in ALS pathogenesis64,66–70. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.