In recent years, the functional benefit of Hmox in preeclampsia has gained increasing importance, in particular, after the publication demonstrating that the adenoviral overexpression of Hmox-1 or direct exposure to CO reduce both basal and VEGF-E-stimulated sFlt-1 release from human umbilical vein endothelial cells (HUVEC), while siRNA-mediated Hmox1 knockdown increases sFlt-1 release (Cudmore et al., 2007). This evidence concerns the gene HMOX1 and preeclampsia.