Prompted by our previous work on the occurrence of elevated levels of cell-free DNA in the circulation of pregnant women with PE (18, 19), we examined whether this disorder is associated with aberrant NETosis and whether such errant neutrophil activity could be the source of this increase in extracellular circulatory DNA. In these investigations, we detected the occurrence of large numbers of NETs in affected placentae (20). This was the first report of aberrant NETosis in a human pathology not related to infection. As NETs were detected directly in the intervillous space, this could lead to occlusion, or infarction, thereby contributing to placental insufficiency proposed to be involved in the underlying etiology of PE (21). Interestingly, NETs were also recently detected in cases of PE associated with systemic lupus erythematosus (SLE) (22), suggesting that these structures may indeed contribute to the development of this enigmatic disorder.