Early in the COVID-19 pandemic, decreased angiotensin-converting enzyme 2 (ACE2) activity after infection, followed by rising aldosterone levels and resulting in urinary potassium loss, was suggested as the primary mechanism for hypokalemia in COVID-19 (7) and has since become a commonly invoked theory when discussing this topic (2, 6, 16–20). Here, ACE2 is linked to Hypokalemia.