As the complex pathogenesis of renal failure in patients infected with SARS-CoV-2 [36,37] likely includes the outcome of imbalanced renal RAS [38], it is tempting to assume that the strengthening of the depressor arm of the RAS by means of the administration of ACE2, Ang-(1-7) or other MasR agonists, or inhibiting the pressor arm, for instance with AT1R blockers, might restore the balance between the two arms of the RAS, attenuate disease severity, and perhaps provide renal protection [4,5]. This evidence concerns the gene ANG and acute kidney injury.