FXIII deficiency increases both TG in plasma and circulating prothrombin fragments. GPRP enhanced TG in normal and FXIII recovery plasma, indicating fibrin involvement. GPRP-modified fibrin structure mimicked FXIII deficiency. Modified fibrin structure attenuated the ATI action of polymerizing fibrin. In ROTEM FXIII replacement partially corrected the defect in fibrin clot formation.