The pathogenesis of human lipodystrophy can be roughly characterized as defective adipocyte differentiation, mitochondrial dysfunction including antiretroviral treatment, dysregulation of lipid metabolism, defective DNA damage repair, or abnormal LMNA genes, including the model for Hutchinson-Gilford Progeria Syndrome, termed “laminopathy” [63]. The gene discussed is LMNA; the disease is laminopathy.