Hypercoagulability in RA was previously detected using ROTEM/TEG [45] and was attributed to endothelial dysfunction associated with the expression of tissue factor, as well as inhibition of the fibrinolytic system, which were combined with an increase in blood levels of inflammatory reactants, such as C-reactive protein and fibrinogen [25,29,46]. The gene discussed is F3; the disease is endothelial dysfunction.