This is supported by some evidence such as (i) the chronology between raised insulin resistance and the growth of fetoplacental unit which is accompanied by increased production of these hormones, (ii) the similarity of metabolic changes after administration of these hormones to nonpregnant individuals having the metabolic dysregulation of GDM, and (iii) impaired glucose uptake after exposure of insulin-sensitive cells such as adipocytes caused by pregnancy hormones [25]. The gene discussed is INS; the disease is gestational diabetes.