Mutations in TMEM43 resulting in emerin degradation or its improper delocalization from the nuclear membrane resulting in disruption of the LINC complex have been implicated in the development of EDMD-related myopathy, which may present clinically with muscular dystrophy, joint contractures, and cardiomyopathy [1,8]. This evidence concerns the gene EMD and Emery-Dreifuss muscular dystrophy.