Results from these mouse models have consistently demonstrated that AS160-KO compared to wildtype (WT) controls were characterized by: whole body insulin resistance without diabetes; insulin resistance for glucose uptake by most skeletal muscles studied; insulin resistance for glucose uptake by WAT and white adipose cells; unaltered activation of proximal insulin signaling as indicated by Akt phosphorylation in skeletal muscle and WAT; and reduced GLUT4 protein abundance in WAT and most skeletal muscles studied [18, 19, 22–24]. The gene discussed is INS; the disease is diabetes mellitus.