Among them was VCP, which plays a prominent role in ubiquitin-based degradation and can cause rare forms of ALS.33 We showed that VCP accumulates with mutSOD1 in the affected motor cortex of ALS patients and exhibits a different interactome in mutSOD1 neurons, while exogenous expression of VCP within in vitro and in vivo disease models alleviated mutSOD1 toxicity. The gene discussed is UBC; the disease is amyotrophic lateral sclerosis.