It has been reported that during SARS-CoV-2 infection: (1) the local levels of angiotensin II (Ang II) increase, acting on angiotensin II type 1 receptors (AT1), and thus increasing arterial pressure; (2) there is endothelial dysfunction in the cerebral vessels in the CNS, which increases the risk of cerebral hemorrhage; and (3) the generation of Ang (1–7) decreases, preventing the vasodilator, neuroprotective, and antifibrotic effects of Ang (1–7)/Mas receptor signaling [122,123]. The gene discussed is AGT; the disease is endothelial dysfunction.