Hence, it is still unclear whether SARS-CoV-2 infection of the endothelium is a plausible mechanism for thrombosis in COVID-19, or whether thrombosis can be sufficiently caused by endotheliopathy alone or in combination with activation of the complement pathway, SARS-CoV-2 induced autoimmunity, or activation of the renin–angiotensin–aldosterone system [46]. The gene discussed is REN; the disease is COVID-19.