Together with earlier data identifying HSPs as direct targets of the key myogenic transcription factors MRFs and MyoD, and considering that mutations in these chaperones are causative for neuromuscular diseases characterized by NMJ degeneration and muscle atrophy, these data highlight the need to better understand whether/how HSPs participate in the maintenance and repair of NMJ (Figure 1). This evidence concerns the gene MYOD1 and neuromuscular disease.