Activation of hemostasis is a major event occurring in Covid-19 patients with severe complications and a need for intensive care or resuscitation. From the Yang report, DIC develops in most patients with a fatal outcome, whilst it remains rare in those who survive [1]. The extensive tissue damage, especially in the lung, and the multiorgan failure can be causes for this extensive blood coagulation activation. Use of an anticoagulant therapy, as, for example with low molecular weight heparin, improves the patients’ outcome and reduces lethality [3,4]. Many coagulation assays are impacted with prolonged prothrombine time (PT) or activated partial thromboplastin time (APTT), reduced antithrombin (AT), elevated DDimer, thrombocytopenia, associated with leucopenia, and low lymphocytes [14]. Mechanisms that cause this direct blood activation can be multiple, and involve the damaged tissues’ debris or released procoagulants, or exposure of activating surfaces to blood circulation in damaged organs. The amplified immune response itself, with inflammation and cytokines release and the cross talks with other response modifiers, can contribute to hypercoagulability. The entry mode for SARS-CoV-2 in infected cells leads one to suspect the involvement of all side effects of a RAAS dysfunction.