Thus, considering that both the patient and her son were born normal, and that lipodystrophy developed in the patient after the onset of puberty, our in vitro results support the idea that lipodystrophy caused by the LMNA R133L mutation is most likely attributable to an inadequacy in the capacity of adipocytes to self-renew, as was apparent in FPLD-transgenic mice with the LMNA R482Q mutation [4]. The gene discussed is LMNA; the disease is lipodystrophy.