In particular, diabetes‐driven inactivation of phosphorylated eNOS (on Ser‐1177), mediated via O‐linked attachment of β‐N‐acetylglucosamine (O‐GlcNAc), has been shown to cause eNOS uncoupling and reduced NO formation in endothelial cells.11 Additionally, the oxidation of tetrahydrobiopterin (BH4), an essential cofactor utilised by eNOS to form NO, leads to eNOS uncoupling. Here, NOS3 is linked to diabetes mellitus.