D-4F treatment evokes a vascular protective role in LPS-induced acute lung injury by improving the endothelial progenitor cell (EPC) numbers, differentiation, and function, and decreasing plasma levels of the pro-inflammatory mediators such as TNF-α and ET-1 partially via the PI3K/AKT/eNOS signaling pathway (115). This evidence concerns the gene AKT1 and injury.