In glucose-rich environment such as hyperglycemia, TAMs possess upregulated GLUT1 expression, thus enhancing their glycolysis and immunosuppressive functions. In low glucose but lipid-rich environment such as obesity-related TME, TAMs take full advantage of fatty acids to maintain immunosuppressive functions. The gene discussed is SLC2A1; the disease is obesity due to melanocortin 4 receptor deficiency.