Since the identification of mutations in lamin genes that cause cardiac and skeletal myopathies in the late 1990s and early 2000s, coined ‘laminopathies’, the nuclear lamin field has received considerable attention using cellular and mouse models to try and uncover the pathophysiological mechanisms (Bonne et al. 1999, 2000; Fatkin et al. 1999; Worman 2012; Worman et al. 2009). This evidence concerns the gene LMNA and skeletal muscle disorder.