A genetic-based deficiency in leptin synthesis in mice also results in pathological alterations in growth plate architecture, a mild form of osteoclast-rich osteopetrosis, and bone compartment-specific abnormalities in cancellous bone microarchitecture [2,12,29], all correctable by leptin replacement [10,12,20,30,31]. The gene discussed is LEP; the disease is osteopetrosis.