Our in vivo experiments in mice infused with genomic DNA or treated with LPS similarly demonstrate that the expression of hPF4 protects animals from plasma-cfDNA-enhanced thrombosis, endothelial activation, and organ injury, consistent with our model (Figure 6) and our prior studies that showed treatment with hPF4 improved outcomes in both murine LPS endotoxemia and cecal ligation and puncture–induced polymicrobial sepsis (32, 35). This evidence concerns the gene ZNF85 and Sepsis.