Indeed, human naturally-occuring LMNA mutations, among other phenotypes of laminopathies, have been shown to be responsible for premature ageing syndromes (Hutchinson-Gilford progeria, HGPS, and mandibuloacral dysplasia, MAD) [1-4], lipodystrophic syndromes (familial partial lipodystrophy of the Dunnigan type, FPLD2) [5,6], and mixed phenotypes [7-10]. This evidence concerns the gene LMNA and Hutchinson-Gilford progeria syndrome.