We demonstrated that there was no apparent difference in insulin-mediated glucose uptake into skeletal muscle between wild-type and AT2 receptor null mice, whereas insulin-induced glucose uptake in white adipose tissue in AT2 receptor null mice was significantly lower than that of control mice.3 It was reported that AT2 receptor-dependent Ang II signaling increases adipose cell mass and glucose intolerance, thereby participating in the deleterious effects of a high-fat diet [8]. The gene discussed is INS; the disease is Glucose intolerance.