A defective RAAS in AKI in form of an impaired renal tubular sodium reabsorption might have led to Hyponatremia.16 Additionally, an impaired non classic RAAS resulting from SARS-CoV-2 interaction with Angiotensin Converting Enzyme-2 (ACE-2) receptors on target cells could be the non AKI dependent mechanism of Hyponatremia in COVID-19 patients. The gene discussed is ACE2; the disease is acute kidney injury.