evidence: Tang et al [7] described the outcome of 183 patients admitted to the Tongji Hospital in Wuhan with RNA detection confirmed 2019-nCoV pneumonia. The authors observed that disseminated intravascular coagulation (DIC) is a frequent occurrence in worsening of COVID-19 pneumonia. Coagulation abnormalities and marked increase of D-dimer were often associated with increased mortality or concomitant severe thromboembolic complications. Surprisingly, the authors noted that in the Chinese population, the prevalence of thromboembolic events was particularly elevated among patients with severe lung failure. Similar prevalence was observed by Cui et al in 81 patients admitted to intensive care units (ICUs), where the prevalence of major thromboembolism was around 25% [8]. Low molecular weight heparin (LMWH) or unfractionated heparin (UFH) at prophylactic doses are associated with a reduced 28-day mortality in more severe COVID-19 patients [9], displaying a sepsis-induced coagulopathy (SIC) score ≥ 4 (40.0% vs. 64.2%, P = 0.029) or D-dimer levels more than six-fold the upper limit of normal (32.8% vs. 52.4%, P = 0.017). Comparably, but slightly higher records of thromboembolic complications (up to about 30%) were observed in Italian patients admitted in ICU (unpublished data). [...] COVID-19 produces a sort of DIC which is usually characterized by hypercoagulability. The exact pathogenetic mechanism of COVID-19-related DIC is unclear, although inflammatory drive and cytokine release may be responsible for the observed coagulation impairment leading to thromboembolic complications. IL-6 may stimulate up-regulation of fibrinogen synthesis by the liver and the virus may bind directly to endothelial cells causing alveolar damage.