In our study, we observed a significant upregulation of proteins with procoagulant properties, such as von Willebrand factor (similar to the results presented previously [5,6]), fibrinogen, and coagulation factor XII; but surprisingly, at the same time, other procoagulants such as thrombospondin-1 (which has been shown to increase in individuals without heart failure [6]) or coagulation factor XI were downregulated. The gene discussed is F11; the disease is heart failure.