Interestingly, we find that most of L-CMD patients harbor mutations in these domains compared with EDMD patients (Table 4), and more specifically 1) in charged residues at e and g positions within the heptad (Table 5), which are involved in ionic interactions between two adjacent Lamin molecules to form a Lamin dimer or 2) in the charged residues localized at the rod domain extremities (Table 6) involved either dimer stabilization or tetramer formation in a mutually exclusive way [4]. This evidence concerns the gene LMNA and Emery-Dreifuss muscular dystrophy.