This hypothesis builds on recent studies providing consistent and identifiable trends in metabolic dysfunction in schizophrenia including evidence of an increased risk of insulin resistance (166), impaired insulin signaling and glucose metabolism (167–173), dysfunctional astrocyte-neuron coupling leading to impaired lactate shuttling and glycolysis (174–179), and abnormal expression of creatine kinase (180, 181). The gene discussed is INS; the disease is Insulin resistance.