Although the ALKBH5-HDAC4-FOXO3 axis is of great interest for the maintenance of skeletal muscle mass, ALKBH5 cannot be considered a potential therapeutic target for the treatment of neurogenic muscle atrophy, since HDAC4 inhibition is protective upon short-term denervation [183], but it is deleterious after long-term denervation [184] or in a chronic condition of denervation, such as in Amyotrophic Lateral Sclerosis (ALS) [185,186]. Here, FOXO3 is linked to amyotrophic lateral sclerosis.