However, this working model cannot fully explain why some of the post-insulin receptor signaling pathways, such as ERK1/2, are not compromised as much as the AKT pathway, suggesting that there is an additional unknown mechanism(s) that can selectively impair the insulin receptor-induced AKT pathway, leading to less GLUT4-mediated glucose uptake in relevant organs or tissues including white adipocytes that play a pivotal role in glucose homeostasis and obesity. The gene discussed is AKT1; the disease is obesity due to melanocortin 4 receptor deficiency.