Long-term treatment of adipocytes with TNFα negatively regulates the expression of Glucose transporter type 4 (GLUT4), also denominate SLC2A, which indicates that TNFα may be a key mediator in abnormal gene expression in syndromes that correlate obesity and diabetes and that consequently affect glucose homeostasis [3,5,42]. Here, TNF is linked to obesity due to melanocortin 4 receptor deficiency.