While we did not find significant differences in perinatal outcomes between OSA and non-OSA groups, we did find an association between altered expression of EGR1 and OSA and REM OSA in pregnant women, all of which could support the hypothesis that differential regulation of EGR1 may contribute to increased fetal susceptibility to complications, such as low birth weight and intrauterine growth restriction in the presence of maternal OSA [39]. The gene discussed is EGR1; the disease is fetal growth restriction.