HDAC4 and amyotrophic lateral sclerosis: Given that HDAC4 has well-established functions in skeletal muscle, muscle atrophy is a major symptom of HD and that HDAC4 has been linked to disease progression in an ALS mouse model, it is likely that genetic reduction of HDAC4 in skeletal muscle was a contributing factor to the improved HD phenotypes (Bruneteau et al., 2013).