Previously, we hypothesized that impaired glucose metabolism and mitochondrial dysfunction in BD, characterized by disrupted oxidative phosphorylation and increased glycolysis, are best explained as a result of disruption of a primary insulin signaling mechanism in the brain: the phosphatidylinositol 3-kinase/Protein Kinase B (PI3K/Akt) pathway [1]. The gene discussed is INS; the disease is Behcet disease.