MEGF10 and myopathy: The molecular mechanism of disease in MEGF10 myopathy/EMARDD involves impaired tyrosine phosphorylation [9] and impaired interactions between MEGF10 and the Notch pathway [10, 11], whereas the cellular mechanism of disease appears to involve potential defects in myogenesis, particularly myoblast proliferation [10] and migration [11], consistent with the congenital onset of disease in the classic EMARDD phenotype.