Hypotheses for ACEI/ARB interactions with COVID-19 have generally fallen along two axes: 1) ACEIs and/or ARBs might increase COVID-19 risk and severity by upregulating ACE2 in pulmonary tissue, thus providing greater opportunity for SARS-CoV-2 entry [20]; and, 2) ACEIs and/or ARBs may reduce severity of COVID-19 disease by shunting angiotensin II to angiotensin(1–7) via ACE2, resulting in anti-inflammatory effects that mitigate the cytokine storm associated with severe COVID-19 presentation. The gene discussed is AGT; the disease is COVID-19.