Overall, these data suggest that a substantial decrease in gal-1 expression in early pregnancy may lead to the complete loss of tolerance and result in miscarriage in both species, while a lower level of inhibition of gal-1 expression at the feto-maternal interface, may enable the further progression of pregnancy but with disturbed maternal-fetal immune interactions, leading to preeclampsia and chronic rejection of the fetal semi-allograft. The gene discussed is GAL; the disease is preeclampsia.