Factors coming from the placenta, such as sFlt1 (soluble fms-like tyrosine kinase-1) and sEng (soluble endoglin) believed to contribute to endothelial dysfunction, could be countered by the strength of the maternal endogenous protective mechanisms such as HO-1, ultimately impacting the degree of clinical manifestation. This evidence concerns the gene HMOX1 and endothelial dysfunction.