We reasoned multiple pathways, such as Na+/H+ exchanger 1, AMP-activated protein kinase, Akt, and prostacyclin synthase in endothelial cell, may mediate this biological action of A-SeQDs on DHFR activation because these mediators are involved in endothelial dysfunction in cardiovascular diseases [21–25]. This evidence concerns the gene PTGIS and endothelial dysfunction.