This significant fetal genetic effect was detected even after we extended the model with maternal FTO risk gene variant that had no effect on postload PG levels and also after the inclusion of MTNR1B rs10830963 genotype to the model, due to that this latter variant is the maternal genetic factor most robustly associated with GDM development and antenatal insulin therapy initiation [14, 22]. This evidence concerns the gene MTNR1B and gestational diabetes.