The difference in tolerability to GV between patients with and without DM is complex, however it is likely that GV in patients with DM may reflect underlying variations in insulin secretion or sensitivity, whereas GV in patients without DM during sepsis may represent a survival response through interactions between insulin signaling pathways, particularly the GLUT-4 pathway, and activation of pro-inflammatory cascades during sepsis as proposed in so-called stress hyperglycemia [27, 28]. This evidence concerns the gene SLC2A4 and diabetes mellitus.