The main reasons for this are that many patients with diabetes exhibit greatly reduced insulin responses to GIP and that elimination of GIP signaling promotes resistance to obesity in rodents [19], [20], [21], [22], suggesting that GIPR agonists would be ineffective in restoring β-cell function and may increase obesity in patients with type 2 diabetes. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.