This has, for example, been shown in amyotrophic lateral sclerosis (ALS), where upregulation of miR-206 has been shown to be part of a cellular autocompensatory mechanism by promoting regeneration at neuromuscular synapses and slowing ALS progression through the downregulation of HDAC4 expression [9]. Here, HDAC4 is linked to amyotrophic lateral sclerosis.