Profound hypokalemia in SARS-CoV-2-infected patients has repeatedly been reported [14, 15], albeit at levels far from the current case, and a mechanistic model for this has been proposed [14]: ACE-2 disruption evoked by SARS-CoV-2 tilts the RAAS balance toward the angiotensin-II pathway, thereby enhancing aldosterone production. The gene discussed is AGT; the disease is Hypokalemia.