Using the amyotrophic lateral sclerosis (ALS) mouse model, characterised by deterioration of NMJs and muscle atrophy, Williams et al. have demonstrated that muscle-enriched miR-206 (myomiR) is a key regulator of muscle–nerve interactions and is required for efficient regeneration of NMJ after nerve injury by regulating Hdac4 (Williams et al. 2009). Here, HDAC4 is linked to amyotrophic lateral sclerosis.