Although the precise mechanism is unknown, these observations are in keeping with the notion that oral salbutamol is effective in a subset of genetic congenital myasthenic syndromes (CMS), in particular DOK7- and COLQ-related CMS, and has been demonstrated to improve AChR cluster assembly and neuromuscular junction architecture in a mouse model of MuSK-antibody MG.29 The mechanism of salbutamol in our cohort may resemble its mechanism in CMS, also considering that other, less-specific adrenergic agonists have been successful in some instances of MG.30,31. The gene discussed is DOK7; the disease is congenital myasthenic syndrome.