In fact, on the one hand, it has been shown that GIP is involved in fat accumulation, and GIPR-deficient mice are resistant to obesity (28), but on the other hand, it has been demonstrated that chronic augmented GIP levels in a transgenic mouse model diminish diet-induced obesity as well as increase insulin sensitivity, glucose tolerance, and β-cell function (29). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.