NETs-derived cfDNA exacerbates inflammation by inducing tumor necrosis factor-α (TNF-α) mRNA, while histones trigger apoptosis and act as damage-associated molecular patterns (DAMPs), promoting proinflammatory cytokine release, cytotoxicity, and ROS-mediated endothelial dysfunction, impairing embryo implantation and placental development, ultimately contributing to adverse pregnancy outcomes (7, 30). This evidence concerns the gene TNF and endothelial dysfunction.