This could have been associated with COVID-19-specific mechanisms, such as cardiovascular consequences of unopposed Ang II-AT1R axis (vasoconstriction, renal salt and water retention, increased sympathetic tone), hypoxia and inflammation (3), but also non-specific mechanisms, such as corticosteroid therapy, fluid and hemodynamic management, sleep deprivation and psychosocial stress. This evidence concerns the gene AGT and COVID-19.