Biological macromolecules have unique rheological properties that distinguish them from common synthetic polymers. Among these, fibrin has been studied extensively to understand the basic mechanisms of viscoelasticity as well as molecular mechanisms of coagulation disorders. One aspect of fibrin gel rheology that is not observed in most polymeric systems is strain hardening: an increase in shear modulus at strain amplitudes above 10%. Fibrin clots and plasma clots devoid of platelets exhibit shear moduli at strains of approximately 50% that are as much as 20 times the moduli at small strains. The strain hardening of fibrin gels was eliminated by the addition of platelets, which caused a large increase in shear storage modulus in the low strain linear viscoelastic limit. The reduction in strain hardening may result from fibrin strand retraction which occurs when platelets become activated. This interpretation is in agreement with recent theoretical treatments of semi-flexible polymer network viscoelasticity.