NADPH oxidase is expressed through Nox1 and Nox2, which can generate the superoxide anion that can act on the synthesis of nitric oxide, leading to its inactivation by oxidation in its cofactor, increased degradation of nitric oxide synthesis, or changes in the expression of nitric oxide synthase, potentially causing endothelial dysfunction, in which a decrease in the synthesis of nitric oxide was observed, along with an increase in the activity of vasoconstrictor substances mainly angiotensin II, which supports the results found in our study [26]. The gene discussed is FMO5; the disease is endothelial dysfunction.