This trafficking of substances and also circulating immune cells to the CNS is achieved because HTN increases the permeability of the blood–brain barrier, allowing, for example, the mentioned systemic Ang II to enter the cerebral circulation [122], and, additionally, Ang II can also activate the AT1 receptor on perivascular macrophages (PVMs) in the brain, promoting the pathogenicity of PVM actions to instigate neurovascular dysfunction through ROS production via NOX2 during chronic HTN. The gene discussed is CYBB; the disease is hypertensive disorder.