The data reported so far led us to speculate that in IUGR-PE and/or early-onset PE, low levels of MIF in early pregnancy contribute to the abnormal placentation, insufficiently stimulating trophoblast invasion; while later in pregnancy, it may induce the general endothelial injury both directly and indirectly by stimulating the production of proinflammatory cytokines (Figure 2). Here, MIF is linked to fetal growth restriction.