Since several studies performed in both rodent model of ALS (G86R mutant SOD1 mice) [115] and human postmortem samples have demonstrated a downregulation of histone acetylation in ALS, it has been hypothesized that the maintenance of proper acetylation by using HDAC inhibitors would be beneficial in ALS and in other neurodegenerative diseases [31,116,117]. Here, SOD1 is linked to amyotrophic lateral sclerosis.