Translational studies using exosomes showed a relationship between the epigenetic modulation of glutamatergic function and a brain metabolic dysfunction known as insulin resistance (IR) as showed by an increase and sex-specific phosphorylation in the expression of IRS1, a key marker of the insulin signaling cascade, in discrete exosomes enriched for the neural cell adhesion molecule L1 (L1CAM), a protein highly expressed in the brain [52, 70–72]. The gene discussed is L1CAM; the disease is Insulin resistance.