Indeed, elevated activities of brain Akt and aPKC in DIO/MetS/T2DM mice returned to normal following reversal of hyperinsulinemia, as elicited by correction of hepatic signaling aberrations and clinical abnormalities with liver‐specific aPKC inhibitor, ATM, which did not cross the blood brain barrier.15, 44. Here, AKT1 is linked to hyperinsulinism.