As cortisol has a well-known anti-inflammatory effect, the negative correlations of MS cortisol with UC PAI-1, as well as UC cortisol with MS S100B, UC S100B, and UC PAI-1 in the IUGR group (Table 2), further enhance the hypothesis for the inflammation-mediating role of S100B and PAI-1. The gene discussed is S100B; the disease is fetal growth restriction.