Given its antiplatelet and vasorelaxant effects, reduced NO bioavailability, because of NOX2 induced oxidative stress (Malkov et al., 2020), likely promotes platelet hyperactivation and coagulation that worsens the pro-thromboembolic phenotype observed in the cerebral microvasculature of AD patients (Veitinger et al., 2014; Canobbio et al., 2015; Bose et al., 2019). This evidence concerns the gene CYBB and Alzheimer disease.