Skeletal myoblasts proliferate, express myogenic markers such as myoD and myf5, withdraw from the cell cycle, and upregulate differentiation proteins such as myogenin and myocyte enhancer factor (Mef2) while fusing into multinucleated myotubes.4 In patients with DM1, the myoblasts fail to exit the cell cycle, leading to a delay in myotube fusion.5, 6, 7. Here, MYOG is linked to myotonic dystrophy type 1.