In accordance with our hypothesis that autophagic clearance of toxic aggregates involving UXT–p62 interaction is required for maintenance of motor neuronal health and function, missense mutations in p62 are indeed linked to ALS in human58, and p62 loss-of-function exacerbates motor neuron degeneration in ALS models in mouse59 and zebrafish60. Here, UXT is linked to amyotrophic lateral sclerosis.