Supporting this finding, it was observed that co-expression of mutant and wild-type human SOD1 increased the solubility of mutant misfolded SOD1 species leading to greater cellular toxicity [28], demonstrating that the soluble form may be an earlier contributor to ALS pathogenesis whilst aggregate formation may represent a cellular defence mechanism [28]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.