Excess production of O2•– or H2O2 through NOX‐dependent mechanisms is thought to lead to eNOS oxidation, monomerization, or uncoupling, and to sGC oxidation, promoting ED and ultimately contributing to conditions such as heart failure and hypertension (Loperena and Harrison 2017; Daiber et al. 2021). This evidence concerns the gene NOS3 and Hypertension.