Lastly, the inhibition of the kinase upstream of AMPK, termed liver kinase B (LKB)1, by the lipid peroxide, 4-hydroxyl-2-nonenal (HNE) [117,118] could provide a connection between excess reactive oxygen species and the inhibition of an LKB1-AMPK-eNOS signaling cascade that causes reduced NO bioavailability and impaired vasodilatory responses in hypertension [95]. This evidence concerns the gene PRKAB1 and Hypertension.