Infection with SARS-CoV-2 can lead to decreased NO production and utilization by a number of mechanisms, including direct infection of endothelial cells, amplification of the detrimental effects of the angiotensin-converting enzyme (ACE)/angiotensin II (AngII)/angiotensin II type 1 (AT1) axis following down-regulation of angiotensin-converting enzyme 2 (ACE2) expression, and further development of the hyperinflammatory state as a cytokine storm (Dominic et al., 2021; Fang et al., 2021; Ferrari and Protti, 2022; Montiel et al., 2022). This evidence concerns the gene AGT and infection.