evidence: Two interrelated and mutually reinforcing phenomena, that is, thrombosis and inflammation, are together believed to result in disseminated intravascular coagulation (DIC) and consumption coagulopathy as a terminal event in COVID-19,[2627] which is far more likely in nonsurvivors (71.4%) compared to survivors (0.6%).[28] In a recent report from Italy, hospitalized COVID-19 patients had arterial and venous thromboembolic complications, occurring at a cumulative rate of 21%, and DIC as a secondary outcome was present in 2.2% cases with associated elevated D-dimer levels indicating inflammatory and procoagulant state in these patients, particularly in those patients who succumbed to their illness.[29] Latest literature showed that COVID-19 acute respiratory distress syndrome (ARDS) patients experienced much higher (11.7%) rate of thromboembolic complications compared to non-COVID-19 ARDS patients.[30] A recent series on 12 COVID-19 autopsy cases reported deep-vein thrombosis in seven cases, in which venous thromboembolism was not suspected antemortem.[31] Apart from hemostatic functions, both coagulation factors and platelets also act as an immunomodulator through their pro-inflammatory properties.[32]