As the pathophysiologic mechanism of GDM is similar to T2DM in which insulin resistance and chronic inflammation are the most important pathophysiological basis, and elevated chemerin expression has been shown to contribute to the development of insulin resistance and low-grade chronic inflammation [8–10], it is possible that chemerin involved in the pathophysiologic mechanism of GDM is by increasing insulin resistance and promoting subclinical inflammation. The gene discussed is RARRES2; the disease is Insulin resistance.