Consistently, LMNA mutations have also been shown to contribute to biophysical defects of laminopathic cells by altering Lamin A “interactome,” either by disrupting the interaction with specific binding proteins or creating new association pathways; for example, the truncating myopathy-causing Δ303 LMNA mutation disrupts the ability of Lamin A/C to bind to matrin-3, altering the connection of the nuclear lamina with the nucleoplasmic content and the structure of the nuclear lamina itself (Depreux et al., 2015). This evidence concerns the gene LMNA and myopathy.