The overarching theme then, borne out by further experiments on known fALS mutations, is that metal-free SOD1 is a cause of ALS, and that some mutants associated with the disease may be more prone to oligomerize in vivo due to alterations in metal binding or the stability of that binding (Banci et al., 2008). Here, SOD1 is linked to amyotrophic lateral sclerosis.