The rationale behind the role of insulin resistance during infection has been provided by in vitro experiments showing that the activation of WBCs leads to the increased expression of glucose transporters (GLUT1, GLUT3 and GLUT4 isoforms) on the plasma membrane; the expression of GLUT3 and GLUT4 and glucose transport are further augmented by increases in insulin levels within the physiological range [72]. This evidence concerns the gene SLC2A3 and infection.