A closer analysis of inflammation in retained placenta should also include “downstream” products of activated inflammatory pathways such as tissue tumor necrosis factor-alpha, placental interleukins, cyclooxygenase-2, and markers of apoptosis as well as other triggers of inflammatory response and endothelial dysfunction such as soluble fms-like tyrosine kinase-1 (sFlt-1) [16, 31]. This evidence concerns the gene PTGS2 and endothelial dysfunction.