From a pathophysiological perspective, our data are compatible with the current model of diabetic neuropathy, in which hyperglycemia and dyslipidemia generate oxidative stress, mitochondrial dysfunction, and activation of NF-κB and inflammatory pathways (including TLR4/iNOS) in axons and Schwann cells [40,41,42]. The gene discussed is TLR4; the disease is diabetic neuropathy.