Finally, although not currently linked to ACEs, in ALS, mutant SOD1 (Superoxide dismutase 1) interacts directly with the mitochondrial voltage-dependent anion channel 1, disrupting oxidative phosphorylation and increasing ROS buildup, while in HD, mutant huntingtin impairs mitochondrial fission-fusion dynamics and lowers ATP production, worsening neuronal vulnerability to oxidative stress [53]. This evidence concerns the gene SOD1 and Huntington disease.