Under normal circumstances, pregnant women should secrete adequate insulin through pancreatic β-cells to make up for the difference in sensitivity of tissues, resulting in an equilibrium of a normoglycemic state; however, women with GDM are not able to secrete adequate insulin to compensate for the resistance, and thus insulin B receptors are unable to undergo tyrosine phosphitylation [21] (Figure 2). This evidence concerns the gene INS and gestational diabetes.