These observations, and the identification of numerous Nesprin-1 mutations linked to Emery Dreifuss muscular dystrophy, arthrogryposis and dilated cardiomyopathies [16] led to the proposal that Nesprin-1′s main muscular function is to anchor nuclei, disruption of nuclei anchorage and subsequent myonuclei mislocalisation being causal to these pathologies. The gene discussed is SYNE1; the disease is dilated cardiomyopathy.