Additionally, it was recently found that AEA impaired insulin‐stimulated AKT phosphorylation and decreased glucose uptake in skeletal muscle cells,47 while CB1R antagonism enhanced insulin responsiveness in skeletal muscle.48 Therefore, CB1R antagonists that have poor brain penetrance (to lessen CNS side effects) might be useful as therapeutic agents in type 2 diabetes where they would be expected to improve β‐cell function, improve glucose uptake into muscle and prevent or reduce hepatic steatosis. This evidence concerns the gene AKT1 and type 2 diabetes mellitus.