Conventional orthosteric ACE2 inhibition strategies exacerbate the angiotensin II accumulation already induced by SARS-CoV-2 infection through receptor internalization [21,22,23,24,25], driving cardiovascular complications, pulmonary pathology, and thrombotic cascades characteristic of severe COVID-19 [26,27,28,29]. The gene discussed is AGT; the disease is COVID-19.