Some of the mechanisms by which aldosterone interferes with insulin signaling and induces vascular dysfunction in obesity and DM2 are already clarified and include increased IGF-1R expression; augmented hybridization of IGF1-R and IR, which are dependent on the degradation of IRS-1 by the proteasome; decreased NO bioavailability and Akt phosphorylation. The gene discussed is IGF1R; the disease is Obesity.