In the context of GDM pathophysiology, based on our findings, in individuals with insulin-resistant GDM, we speculate that the placenta may be unable to produce increasing amounts of IGFBP1 as pregnancy progresses; this deficiency in circulating IGFBP1 could contribute to excessive insulin resistance, and thus to maternal hyperglycemia detected in the late second trimester in this GDM subtype. This evidence concerns the gene IGFBP1 and gestational diabetes.