However, mutant DJ-1 may also accumulate into insoluble cytoplasmic aggregates [14], [15] and acquire a gain-of-function property that may co-exist with its loss of physiological activity, as previously found for mutant HTT in HD [16] and superoxide dismutase 1 (SOD1) missense mutations in amyotrophic lateral sclerosis (ALS) [17]. Here, SOD1 is linked to Huntington disease.