The shortage of insulin signaling or insulin resistance results in the internalization of GLUT4 and a marked down-regulation of membrane GLUT4 (Figure 2), which finally leads to the decreased glucose uptake in cells and hyperglycemia (21, 22) and compensatory increased LCFA uptake to break the equilibrium of myocardial energy metabolism in diabetes (5). This evidence concerns the gene SLC2A4 and diabetes mellitus.