Recent histopathological studies from patients who died from severe COVID-19 indicate the presence of endothelial inflammation [31]; moreover, neuroinflammation during COVID-19 could be partially explained by changes in ACE2 expression at the blood–brain barrier of the vast brain network of capillaries, which could affect the integrity of endothelial tight junctions, thereby allowing passage of cytokines and inflammatory cells. The gene discussed is ACE2; the disease is COVID-19.