Our data correspond well to several previous reports demonstrating alterations in balance between lipid oxidation and oxidative glucose metabolism in cultured myotubes from FPLD patients with LMNA R482W/R482Q mutations and glycolysis dysregulations in HeLa cells with lamin A/C dysfunction as well as in fibroblasts derived from patients with laminopathies [21,56,57]. The gene discussed is LMNA; the disease is laminopathy.