More importantly, the mutations in SOD1 cause alteration in protein stability and their propensity to aggregate, which is similar to TDP-43 and FUS, while also correlating with ALS disease development; this hence implies the intrinsic functional integrity of these proteins needed in vivo, as any instability disrupting their integrity may not only have a bearing on each other, but also on the maintenance of protein homeostasis with the cell. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.