Several models such as conventional and genetically modified C57BL/Ks (db/db) mice, streptozotocin-induced C57BL6/J and ddY mice, spontaneously diabetic WBN/Kob rats, L-fucose induced neuropathic rats, nonobese diabetic (NOD) rats, spontaneously induced InS2 Akita mice, leptin-deficient (ob/ob) mice, high-fat diet-fed female C57BL6/J mice, and genetically modified SDT fatty rats have been shown to develop major pathogenesis of diabetic neuropathy or peripheral diabetic neuropathy; however most of them were not validated either by antidiabetic or antineuropathic drugs. The gene discussed is LEP; the disease is diabetic neuropathy.