Considering the aforementioned data and the fact that GLUT3 has a much higher glucose affinity than GLUT4 [52], we cannot rule out the possibility that the observed GLUT3 overexpression, along with GLUT1 upregulation, in the leukocytes of the women with GDM could represent a compensatory mechanism to maintain glucose influx to the leukocytes despite GLUT4 being lost in these cells. This evidence concerns the gene SLC2A1 and gestational diabetes.