We chose two distinct models to address the questions, the well-characterized leptin receptor deficient (dbdb) mouse model of diabetic polyneuropathy [2], [24], and mice lacking the superoxide dismutase 1 (Sod1) gene (Sod1−/−) as a model of in vivo oxidative stress [25], [26], [27], [28]. The gene discussed is LEPR; the disease is diabetic neuropathy.