Interestingly, trophoblasts isolated from GDM placentas also showed an attenuated response to in vitro insulin treatment in terms of dissociation of SERT from the endoplasmic reticulum chaperone ERp44, suggesting that defects in insulin signaling are responsible for the impaired functional expression of SERT on the cell surface in GDM trophoblasts (55). The gene discussed is INS; the disease is gestational diabetes.