Epidemiological studies have suggested the biological molecules contributing to placentalvasculogenesis and controlling maternal blood pressure as the causes or exacerbating factors in preeclampsia (e.g., soluble Fms-like tyrosine kinase (sFLT1) [17], soluble Endoglin (sENG) [18], transcriptional factors such as STOX1 [19], and protein peptidases(ADAMs, MMPs) [20, 21]). This evidence concerns the gene STOX1 and preeclampsia.