Recently, Wu et al.showed that mice selectively expressing CUL3Δ9 (CUL3Δ403-459) in the vascular endothelium (E-Cul3Δ9) exhibit impaired activation of endothelial nitric oxide synthase (eNOS) due to dephosphorylation by CUL3 substrate protein phosphatase 2A (PP2A), culminating in decreased NO biogenesis and endothelial dysfunction [66]. This evidence concerns the gene NOS3 and endothelial dysfunction.