Fig 1: Diagram illustrating the SARS‐CoV‐2 ‐mediated induction of plasma CD40L and P‐selectin levels, and suppression of tissue factor pathway and FXIII. SARS‐CoV‐2 ‐mediated endothelium damage potentially contributes to the elevated level of plasma CD40L (sCD40L) and P‐selectin which induces platelet activation. The activated platelets further releases P‐selectin and sCD40L and provides positive feedback to platelet plug formation and platelet‐mediated thrombin generation. An attenuated level of TFPI activates the tissue factor pathway which likely boosts thrombin level and enhances platelet activation. The elevated level of fibrinogen in COVID‐19 patients likely provides the required fibrin however, a decreased level of FXIII indicates the defective fibrin polymerization which potentially results in unstable thrombi formation and embolization. Moreover, an elevated level of PAI‐1 prevents fibrinolysis in moderate COVID‐19, however, an increased level of tPA in severe COVID‐19 likely induces hyperfibrinolysis in turn increased level of D‐dimer formation. +, positive feedback; FXIII, factor XIII; PAI‐1, plasminogen activator inhibitor‐1; sCD40L, soluble CD40 ligand; TFPI, tissue factor pathway inhibitor; tPA, tissue plasminogen activator. Dotted lines; not known if direct or indirect regulation, Solid line; direct regulation