A striking feature of patients who develop severe COVID-19 is the prevalence of specific forms of vasculopathy, thrombotic microangiopathy, and intravascular coagulopathy, as suggested by clinical evidence.[36,37] It is inferred that this condition is due to the direct link between hemostasis and the inflammatory and immunological responses, suggesting that SARS- CoV-2 impairs innate and adaptive antiviral responses, triggering hyperinflammation and deregulating the renin-angiotensin-aldosterone system (RAAS).[38] Thus, acute lung injury can lead to hypoxemia. This evidence concerns the gene REN and COVID-19.