To further investigate the mechanisms by which PFKFB3 contributes to endothelial dysfunction and decreased NO bioavailability, we transduced HAECs with NOX1 adenovirus (in addition to its coactivators NOXA1 and NOXO1) and either GFP (control) or wt-, cyt-, or KD-PFKFB3 (Figure 6A). This evidence concerns the gene NOX1 and endothelial dysfunction.