The occurrence of these comorbidities could be related to the following main mechanisms: (1) activation of endothelium cells by pro-inflammatory cytokines, known as the “cytokines storm"; (2) viral infection-mediated endothelial cells damage and extrinsic pathway activation, through inducing TF expression; (3) decrease plasma activity of ADAMTS 13 metalloproteinase, with subsequent accumulation of vWF multimers in plasma and formation of platelet microaggregates in the circulation; (4) and RAS unbalancing mediated Ang II high plasma levels following by thrombin activation (Fig. 1). The gene discussed is TF; the disease is viral infectious disease.