Although these observations demonstrate potential for DOK7 gene therapy in these myopathies with NMJ defects, we suspected that this therapy might also benefit motor neurodegenerative diseases, because muscle‐specific overexpression of Dok‐7 activates MuSK and enlarges not only the postsynaptic apparatus but also presynaptic motor nerve terminals at NMJs, which might counteract degeneration, or size reduction in particular, of the terminal (Inoue et al, 2009; Arimura et al, 2014). Here, MUSK is linked to myopathy.