Congenital partial lipodystrophies resulting from mutations in LMNA, coding for nuclear envelope components, lamin A and C, or from mutations in gene coding the peroxisome proliferator activated receptor γ (PPARG) are characterized by abnormalities in the lipid profile (hypertriglyceridemia, low HDL-cholesterol), hirsutism, acanthosis nigricans, and hypertension [55, 56]. This evidence concerns the gene LMNA and lipodystrophy.