Some studies indicate that glucose metabolism is compromised in schizophrenia [141, 142]; hence, detection of the insulin receptor and Akt activity in postmortem brains of schizophrenic patients, in insulin knockdown HEK cells and in a mouse model of insulin resistance, revealed a significant reduction in the number of insulin receptors and in the total and active forms of Akt. This evidence concerns the gene AKT1 and schizophrenia.